BIOL1020 Semester 2, 2008

Genetically Modified Tomatoes May Help Prevent Cancer…

2009-08-28T10:39:00.001+10:00

For many years, dietary consumption of anthocyanins has been associated with protection against a broad range of human diseases. Scientists have now found a way to engineer anthocyanin accumulation in tomatoes by genetically modifying the fruit to express two transcription factors of snapdragon – a plant containing high levels of anthocyanins.

Expression of the two transgenes has enhanced the hydrophilic antioxidant capacity of tomato fruit threefold and resulted in fruit with intense purple coloration in both peel and flesh. In a pilot test, mice engineered to develop cancer were fed a diet supplemented with the high-anthocyanin tomatoes and showed a significant extension of life span than those mice fed on a diet supplemented with normal tomatoes. These promising test results have prompted further experimentation with what is being known as the ‘super tomato’; the next step is to investigate how the antioxidants actually affect the tumours to promote better health.

2009-08-28T05:32:00.003+10:00

Too lazy to do work? Try D2 gene therapy.

Using gene therapy to block cells receiving dopamine was shown by U.S. researchers to be a way of transforming lazy people in to more efficient and hard workers! The theory behind this seemingly incredible treatment is of the function of dopamine. Dopamine is known as a chemical messenger associated with rewards, movement and other functions. By using gene therapy to block the D2 gene, which creates receptors of dopamine, the cell won’t receive dopamine. The researchers experimented on monkeys. Comparing the results before and after the therapy the researchers claim that "[the monkeys] work more efficiently, make fewer errors, as they get closer to being rewarded. But without the dopamine receptor, they consistently stayed on-task and made few errors, because they could no longer learn to use visual cues to predict how their work was going to get them a reward."

This study of the basis of work and reward may seem trivial at first sight, but however may lead into major breakthroughs in medicine. For example people who are depressed feel that they have nothing worth working for. People with obsessive-compulsive disorder work incessantly even when they are repeated. In mania, people will work feverishly for rewards that aren’t worth the trouble for most of us. By altering the D2 receptors via gene therapy, it may be possible to cure these diseases.

Andy Hua (42028095)

http://www.abc.net.au/science/articles/2004/08/13/1175754.htm

Stanford Scientists Explore New Way to Change Cell's Identity.

2009-05-11T08:17:00.002+10:00

Experiments into influencing stem-cell development are not uncommon today, but scientists from the University of Stanford have completed a study into altering gene expression in fully differentiated cells. The experiment combined mouse muscle cells with human skin cells creating a hybrid 'heterokaryon'. From these heterokaryons the effect of the nuclei on each other became apparent. It was observed that in cells where the nuclei from muscle cells were more prevalent, the skin cell nuclei would begin to express muscle genes, and the reverse was true when skin cell nuclei were the more abundant.

This study will allow scientists to better understand how to induce specialized adult cells to revert to a stem-cell-like state in a process called induced pluripotency. Pluripotent stem-cells can be progressed artificially along a number of pathways to reach one of a number of final, fully differentiated states. The experiment also revelas a new alternative to stemcells; encouraging a lateral shift in differentiated cells to an alternative, but still fully differentiated, state.

The article can be found here.

James Cochrane (42014678)

Ruppy the glowing puppy: World's First Transgenic Dog

2009-04-28T17:15:00.001+10:00

Seoul National University, who brought us the world’s first cloned dog Snuppy in 2005, have now created the world’s first transgenic dog, a cloned Beagle puppy named Ruppy. Ruppy’s embryo was inserted with a cloned fibroblast cell which contained a gene from a sea anemone. This gene expresses a red fluorescence and so Ruppy glows red under ultraviolet light.

The scientists at the university used a retrovirus, to transfer the sea anemone gene into the cloned dog fibroblast cell. The virus inserted the red fluorescent gene into the nucleus of the dog cells, and that nucleus was then removed and placed in another dog’s egg cell. The egg cell placed in a Petri dish where it was left to divide for a few hours and then the whole embryo was transplanted into a surrogate mum.

The success rate of cloning the dog embryo’s was not very high, with only 7 pregnancies from 344 embryos- a 1.7 per cent success rate. From those 7, only 5 dogs made it to healthy puppyhood, Ruppy being amongst them.

However, the scientists couldn’t control where the virus inserted the gene, as has been achieved in transgenic rats and mice, therefore limiting the possible medical benefits that Ruppy and co. could have brought about. “Gene targeting” brings experimentation advantages because it allows animals to be created that either lack a specific gene or have a mutation on that gene. The team is working on adapting a method of “gene targeting” currently used in cows and pigs, so that it can be used on transgenic dogs as well.

Ruppy has had mixed reception amongst researchers currently studying disease through animal modes. While some scientists feel the creation of a transgenic dog equips scientists with new tools to study disease, due to their long life span and reproductive cycle, others feel that transgenesis is too time consuming, costly and with negative public perception of laboratory reared transgenic dogs; these factors will limit the amount of benefit to be gained from Ruppy.

For original article by Ewen Callaway 23 April 2009:

http://www.newscientist.com/article/dn17003-fluorescent-puppy-is-worlds-first-transgenic-dog.html

By Morgan Brain 41237537

Reading Disability and ADHD: Environment and Genetics

2009-04-22T09:15:00.003+10:00

Environment and gene interactions, also known as nature and nurture have been widely debated throughout academic research. This is due to the implications of findings being especially significant in regards to treatment and prevention of various medical problems. Reading disability (RD) and attention deficit hyperactivity disorder (ADHD) are two well known developmental disorders with onset commonly during childhood and adolescence. These disorders can occur both individually and comorbidly, and as such there has been much research regarding the environmental and genetic components. RD and ADHD have heritability factors of 58% and 76% respectively (Pennington, McGrath, Smith, Willcutt, Friend, DeFries & Olson 2009). The interesting aspect with these disorders is that RD is more likely to develop within a favourable environment which can include factors like high resilience and high parental education. ADHD is complementary as it is more likely to develop within a risk environment which can include factors like a high stress home life and prenatal smoke exposure. The aim of this study was to determine the environmental factors that facilitated genetic expression that triggered these disorders. This information can then provide possible preventative measures to be taken when a child is known to be at risk.

Twins are the ideal candidates for gene and environment interaction studies, as they are the only method for controlling for numerous environmental and genetic variables. The study used monozygotic and dizygotic twins to examine behavioural genetics. This was measured by the presence or absence of features like inattention and word recognition. This was in participants both at risk and not at risk. Although dopamine transgression is known to be related to ADHD and neuronal migration related to RD, these factors were inferred rather than directly measured - as would have been the case in molecular genetics (Pennington et al. 2009).

It was concluded that there was a trend in RD such that it appeared to develop in the presence of lower parental education, a risk environment however neither had significant results. Rather than non-significant results indicating that there are in fact no genetic and environmental links it was stated that it was the consequence of previous literature’s inconsistencies concerning behavioural genetics. Many variables had not adequately been defined prior to the study which confounded the design. For example, the study used a large proportion of participants with a diverse ethnic background as well as SES (socio-economic status) levles (Pennington et al. 2009). These major factors may have affected the results as the participants were not entirely representative of the population and therefore the results could not be generalised. In addition to this, these disorders are not defined within spectrum. They are categorical, such that there are cut-offs to determine whether or not the disorder is diagnosed. Consequently, there may be participants who almost filled the criteria but fell just short and conversely children who only just filled the criteria. This meant that the severity of the disorder was not taken into account which could have significantly affected the results.

Extensive testing is required to determine all of the genetic and environmental factors eliciting the development of RD and ADHD disorders. As such, further in-depth research into all factors possible is necessary before any conclusive results can be considered reliable and valid within the domain of behavioural genetics.

Pennington, B, F., McGrath, L. M., Smith, S. D., Willcutt, E. G., Friend, A., DeFries, J. C. & Olson, R. K. (2009). Gene X environment interactions in reading disability and attention-deficit/hyperactivity disorder. Developmental Psychology, 45, 77-89.

Anna Pritchard s4098124

Is That a New Coat?

2009-04-19T20:03:00.004+10:00

The endemic disease African Trypanosomiasis, more commonly known as African Sleeping Sickness, has been plaguing African countries in epidemic proportions it recent years. Caused by the protozoa of the parasite Trypanosoma brucei, the disease has capability to avoid annihilation by the hosts immune system. Its ability to do so stems simply from changing coats.

The immune system of the infected body manages to wipe out the vast majority of parasitic cells, the remaining cells alter their own DNA and as a result changes it's surface coat. This brings on a new onslaught of infection and usually ends in death. In order to change the DNA, the parasite slices both strands of its double helix. Towards the end of the parasite's chromosomes (15-20 regions) are Variant Surface Glycoproteins (VSG). The VSG controls the surface coat of the parasite, by slicing the DNA at the end of the chromosome and thus shortening the VSG changes the surface coat. The changed coat is able to avoid detection and begin to attack the body again.

This has always been the theory to how Trypanosoma brucei has avoided detection, it was not until recently that this was proven. This was done by artificially putting breaks in the VSG and above the VSG and determing if the coat changed. DNA-cleaving enzymes (Restriction Enzymess) extracted from yeast were used in this process.

This is an important discovery in the realms of health and biological sciences. New drugs can now be formulated to help prevent the DNA splicing to commence and allow the immune system to completely wipe out and parasite.

Dale Gibson - 42065326
http://www.sciencedaily.com/releases/2009/04/090415141210.htm

Plant Provides Hope for Genetic Diseases

2009-04-18T11:14:00.003+10:00

A recent breakthrough has given doctors new hope in finding a cure for genetic diseases including Huntington's Disease, Freidreich's Ataxia and Fragile X Syndrome. These diseases were included in the study as they are all genetic diseases caused by triplet repeating extensions in the subject's DNA. Another criteria for their inclusion in the study is that they often become more severe over generations and have long timeframes involved which makes studying the diseases in a human very difficult.

The researchers discovered that a plant, Arabidopsis thaliana, has the same repeat patterns that are found in these human diseases. Researchers suggested that the plant may be used as a model for future research especially into increasing our understanding of how these repeat patterns change over generations. The plant provides hope especially has the disease it has applications for become more severe over generations and have long time spans. The plant model offers a much shorter time span and allows for very quick study of mutations over several generations. Overall, the research provides much hope for genetic research not only for the diseases studied in this research but for many more issues as it has concluded that human genetic patterns occur in as distant species such as plants.

Original Text: http://www.uq.edu.au/news/?article=17223

2009-04-01T00:55:00.003+10:00

ARE YOU A CHIMERA? WILL YOUR BABIES GENETICALLY CLASSIFIED AS YOUR OWN BABIES?

Imagine if you were denied custody of your own daughter because she didn’t share the same DNA. What if you genetically didn’t share much in common with your mum? Would she still be your mum?

The problem is becoming increasingly more common in DNA testing and there is an explanation. Each related individual are just made up of different sets of calls consisting of different DNA. They are called chimeras.

A human chimera consists of two sets of cells with DNA as similar as that of two siblings. A chimera results when two fraternal twins fuse together at an early stage in development.

This factor is possible due to the early principle of life. At the beginning, the building blocks of embryos are embryonic stem cells (ES). These cells have not yet committed to any specific category of cells therefore missing cells are tolerated and expected. This stage also allows cells to be taken out or combined which creates a chimera. This process of combing two of the ES cells has no effects or consequences for the new chimera unless they are o different sexes (may cause chimera to become a hermaphrodite).

When testing for DNA between family members should usually be a simple and easily justified case, however, for chimeras problems develop. As different body cells will posses different DNA, the test can possibly present incorrect results and a mothers children can be showed to be a nephew or niece instead of a son or daughter.
Although chimerism is very rare, its becoming increasing more presents in DNA testing. This rare condition presents problems in the future of DNA testing and infers that scientists are going to need to be more careful as to how they interpret results!
The US Government as now abolished any experimental testing that involves the production of chimeras.

Anorexia-Not all in the mind

2009-03-30T22:28:00.000+10:00

A recent study by researchers in a US lab have begun to discover that anorexia nervosa, a disease thought to be purely psychological and brought on from environmental factors may in fact have its basis in genetics. This study found that someone who has a relative who suffered from anorexia nervosa is 12 times more likely to suffer from the condition than anyone else. Anorexia nervosa is an incredibly harmful disease in which the sufferer has a distorted body image of themselves, causing them to perceive themselves as fat and thus avoid food, leading to starvation, malnutrition and eventually, if not treated, death.

It has always been believed that people develop anorexia through environmental pressures, and that if pressure was not put on society to be thin, we wouldn't face this problem. This new research however, suggests it may be a combination of both nature and nurture which brings on this illness. As Dr Johnson, one of the principal researchers on this project said, "Genetics loads the gun, environment pulls the trigger." Although this identified only that these people had an increased chance through their genetic disposition, the researchers also found that the group most at risk is young girls, aged between around 11 to 14.

Where is my gene hiding?

2008-11-04T11:48:00.003+10:00

Gene mapping is a method of finding the location of a genes and whether they are located on the same chromosome or linked.

To map genes, a certain species of fruit fly, Drosophila melanogaster is examined.

Firstly, we have to identify the phenotypic character of the Drosophila. The normal phenotype is called the wild type and will be denoted with a + while the opposite is called mutant phenotype. In this case, the character identified is the body color and the wings. Wild type Drosophila has grey bodies and normal wings while the mutant has black body and vestigial wings.

To see how linkage between genes affects the inheritance of characters, a homozygous dominant female Drosophila is crossed with a homozygous recessive male. A heterozygous F1 dihybrid will be produced. By observation, all the F1 dihybrids possess the phenotypic character of the wild type flies.

Following that, the F1 female dihybrids are crossed with the male true-breeding homozygous recessive parent fly. This method is called test cross as suggested by Mendel. From this, we can identify the genotype of the female parent and the alleles that are derived from the parents.

In this process, all the sperm will donate recessive alleles while the ova’s allele will be expressed as the phenotypic character of the offspring. Thus, by observing the phenotype of the offspring, we can tell if the genes are on the same chromosome or not.

Since chromosome is the unit of transmission during meiosis, linked genes are unable to undergo independent assortment as predicted by Mendel’s law. By using the Punnette square analysis, we observed that most flies appeared as parental phenotype. However, there are also some offspring that have traits that doesn’t match the parents (recombinants).

Theoretically, all alleles on a single chromosome should be transmitted as a unit during gamete formation. Hence, from our experimental results, we can conclude that body color and wing size are usually passed down together but only partially linked.

This is due to crossing over during meiosis where the parent’s chromatid breaks at certain points and rejoin causing a transfer in genetic information. The recombinant chromosome is passed on to gametes after subsequent occurrence of meiosis. Generally, it has been proven that the 2 genes are on the same chromosome.

Assuming that crossing over is random, the extent for this to occur is roughly equal at all points on the chromosome or proportional to the distance between the genes. Therefore, the higher the recombinant frequency, and the further apart the two genes are, the higher the chances for a cross over to occur. However, the maximum value for the recombinants is only 50 %.

Next, a linkage map is constructed based on the recombinant frequency. The distance between the genes are expressed as centimorgans where one map unit is equal to 1% recombinant frequency. Recombinant frequency is calculated by taking the total number of recombinants divided by the total offspring and then multiplied by 100. The genes are then arranged on the chromosome linearly based on their recombinant frequencies.

To conclude, gene mapping is a useful method for us to manipulate genes for better usage in the future.

41872460

2008-10-30T14:02:00.003+10:00

In the first experiment of its kind conducted in nature, a University of British Columbia evolutionary biologist has come up with strong evidence for one of Charles Darwin's cornerstone ideas which is adaptation to the environment accelerates the creation of new species.

"A single adaptive trait such as color could move a population towards the process of forming a new species, but adaptation in many traits may be required to actually complete the formation of an entirely new species," says UBC post-doctoral fellow Patrik Nosil, whose study is just published. "The more ways a population can adapt to its unique surroundings, the more likely it will ultimately diverge into a separate species."
Nosil studied walking-stick insects in the Santa Barbara Chaparral in southern California. Stick insects cannot fly and live and feed on their host plants. Different "eco-types" of walking-stick insects are found on different plants and exhibit different color patterns that match the features of their host plants. For example, insects of the cristinae eco-type, which feed on plants with needle-like leaves, have a white line along their green bodies.
By displacing some eco-types away from their customary host plants and protecting others from their natural predators, Nosil found that color pattern alone could initiate speciation, while natural selection on additional adaptive traits such as the ability to detoxify different host-plant chemicals are required to "seal the deal," or complete the speciation process initiated by differences in color pattern.
"Natural selection has been widely regarded as the cause of adaptation within existing species while genetics and geography have been the focus of most current research on the driving force of speciation," says Nosil.
"As far as advancing Darwin's theory that natural selection is a key driver of speciation, this is the first experiment of its kind done outside of a lab setting. The findings are exciting," says Nosil.

The original article is here. http://www.plosone.org/article/info:doi/10.1371/journal.pone.0001907

41874996

Transexuality related to genes!

2008-10-30T01:50:00.006+10:00

For decades, there have been many debates on whether transexuality is related to genes. But there is always a social stigma which indicates that transexualism is simply a lifestyle choice.

However, based on Vincent Harley, a lead researcher of Monash University's Prince Henry's Institute of Medical Research findings, the biological basis on how gender identity develops were explained. They have identified that transexuality may be linked to the androgen receptor (AR gene), which is known to modify the effect of the male sex hormone testosterone. Studies have found out that transsexuals are more likely to have longer version of the AR gene compared to those whom are non-transsexual men. The longer AR gene may have resulted in a less effective testosterone signaling which masculinises the brain during the early foetal development. They claimed that, it is possible that there is a decrease in the testosterone levels in the brain during development which may have resulted in incomplete masculinisation of the brain, causing them to form a more feminized brain and thus a female gender identity.

http://tvnz.co.nz/view/page/411416/2235472

http://www.okdiversity.com/genderbenders/images/transexuals/tiana001.JPG

Tan Qiao Ye (41617223)

The Lean Gene and the ‘Skinny Gene’ Test?

2008-10-28T02:19:00.006+10:00

The lean gene and the ‘skinny gene’ test? Yes, that’s absolutely right. Scientists have now discovered that thinness is a trait that can be inherited, just like one’s skin colour and smile. And as absurd as it may sound, scientists are even taking it a step further by declaring that they are working on a ‘skinny gene’ test that may help women find out how hard they would have to work in order win the war they wage against their weight.

Prof. Gregory Livshits from the Sackler Faculty of Medicine at Tel Aviv University and colleagues from King's College in London, who contributed their findings in this area conducted their study on more than 3,000 middle-aged women in the United Kingdom who belonged to either an identical or fraternal twin pair. Their "total lean mass," one of the three major components of body weight, was measured and compared to markers in their genes.

The results? Well,he found that 50 percent of the time, a woman’s body mass depends on her genetic make-up. The bad news for people who did not inherit the ‘lean gene’ from their parents is that they would always find it harder to stay svelte. However, all is not lost as women can still go against their gene constitution and lose weight. What women should understand, though, is that as they age, there is little that can be done about their weight. A woman’s weight is also complex, especially when age enters the equation. There is yet a lot more to be understood about it.

So it’s best not to get too jealous of your friend's dress size. After all, it may be mostly out of your hands --and in your DNA.

http://www.sciencedaily.com/releases/2008/04/080401120505.htm

Kanmani N.Balasubramaniam, 41592441

Cost of human brain evolution

2008-10-27T17:11:00.004+10:00

Schizophrenia is a common mental disorder troubling modern people. This syndrome includes delusion, hallucinations and disorganized behavior. Scientists have not discovered the cause of this metal problem yet. Until recently, a research group suggested that schizophrenia might be induced by brain evolution.

In the study, scientists focused on the gene expression and metabolic rate of brains. They investigated a group of healthy and schizophrenic human with chimpanzee brains and identity the causes from the data. According to the theory suggested in the past, it was proven that some of the neurological diseases were caused by increase in brain size and metabolic rate during evolution. Scientists in this experiment found that molecular changes in schizophrenia would cause disorganized speech and hearing to the patients. Most of the gene expressions and metabolism were altered in schizophrenic brains. These transformations were mainly triggered by rapid evolution. The brain could not cope with a sudden increase in metabolic demands and resulted in mental disorder.

In my view, this is a great discovery in neurological diseases. It helps doctors to develop a deeper understanding of the cause of disease in order to provide a better treatment to patients. Based on the result obtained, scientists can know more about brain function and use the data to cope with other neurological disorder. More researches should be done in the future.

Reference:

BioMed Central (2008, August 5). Schizophrenia: Costly By-product Of Human Brain Evolution?. ScienceDaily. Retrieved October 27, 2008, from http://www.sciencedaily.com /releases/2008/08/080804222910.htm

Anthea Wong (41598331)

Study Finds Value In "junk" DNA

2008-10-27T14:41:00.008+10:00

DNA is a sequence of gene that contains the genetic instruction, which controls important roles in the function and development of human body. About 5% of human genome is known for its function, but the rest of 95% are still undiscovered. Scientists used to have difficulties in finding the role of these DNA, which later known to be ‘Junk’ DNA or basically a sequence of repetitive DNA that its functions are still not yet discovered.

However, these non-coding pieces are no longer useless, as a University of Iowa study has found evidence that these junk DNA can evolve to a number of exons, which very important in gene regulation. The findings are published October 17 in the open-access journal PLoS Genetics.

In human body, nearly half of the DNA is repetitive DNA, which including transposons, a segment of DNA that can move around to different position of genome in a single cell. A type of transposons called retrotransposons that have the ability to synthesize copy of RNA, consists of a common element called Alu.

These Alu elements created hundreds of exons in human body and scientists wanted to know what role that these exons play in regulation of gene . Thus, by using a high density exon microarray, Alu is being investigated and the result showed Alu-derived exons in 11 human tissues and also its interesting functions and its expression.

One interesting aspect about Alu element is it expressed at a high level in the human muscle. The presence of this particular Alu element in human muscle resulted in human-specific change from a diverged evolutionarily that occurred between human and chimpanzees. This explained that Alu only available in human but not human or non-human primate tissue and its essential function in human muscle.

Citation:
Study Finds Value In "junk" DNA 2008, Medical News Today, http://www.medicalnewstoday.com/articles/126015.php

41818507

Detecting genetic drift versus selection in human evolution

2008-10-24T13:58:00.002+10:00

Many factors can shape the way species' undergo evolution. These include new mutations, non-random mating, genetic drift and natural selection. Over millions of years, a single species could evolve through each of these factors many times, which is why it is so interesting to research. It becomes particularly interesting when investigating the lineage of the genus Homo, or more commonly known, our own lineage.

Rebecca Ackermann and James Cheverud decided to launch a paleoanthropological investigation into the heritage of the human race to try and decipher when and how we evolved and what factors were more prominent in these evolutions. They achieved this by taking samples of fossils mainly from Kenya and South Africa and reconstructing them using a number of different computer programs and methods. They then applied a number of equations to determine whether the facial morphology was affected by genetic drift or not.

Out of the four analyses on the same set of fossils, only one showed that genetic drift was the main factor for evolution, with two others promoting selection and one being unable to tell. This was because there was far too much variation in the facial features for the cause to be genetic drift alone, although it definitely was a minor factor in all cases. This conclusion leads the researchers to believe that there is much more research to be done in this area and it is quite possible that it will be discovered that genetic drift was a major factor for the variation. For our sakes, I'd like to think that we didn't become what we are today through random chance and instead a more stable plan, however with modern science as it is, it is very possible that this research could be advanced in the not too distant future.

For the article:
http://blackboard.elearning.uq.edu.au/webapps/portal/frameset.jsp?tab_id=_151_1

Andrew French
s41760174

Gene mutation in Worms key to Alcohol Tolerance

2008-10-24T13:19:00.000+10:00

The article is about discovery made by group of researchers from Oregon Health and Science University. They discovered that the gene mutation found in worms and mice can lead to alcohol tolerance. The type of the gene mutation is the one which can result in a change in characteristics of one of the amino acids that build up our nervous system. This alteration thus, allows the nervous system of the body to become less sensitive to the alcohol.

I thought this discovery may lead to invention of medication which allows a person with exceptionally low alcohol tolerance to be able to enjoy their drinking more. Although this might be a great profit to beer and spirit industries, concern will remain in the fact that people will not be able to know their limits for alcohol consumptions. I hope that this discovery will lead to something useful in our lifestyle.

Genetically mutant worms consume more alcohol

2008-10-24T13:18:00.005+10:00

The researchers in Oregon Health and Science University discovered that there is a connection between genetic mutation in worms and alcohol tolerance. They have specifically looked at the gene responsible for communication between nerve cells. This gene normally determines how the amino acids will arrange themselves into a protein called UNC-18 and the nervous communication is facilitated. With this gene mutant, the researchers found that there was a significant change in which the nerve cells of the worms communicate. As a result, the worms showed less sign of alcohol influence and consumed more alcohol.

Biomedical Science Professor Bob Burgoyne explains, alcohol consumption can affect the nervous system in several different ways. The body becomes alert with low alcohol concentration but as more alcohol accumulates, the body starts having a motor dysfunction and lack of coordination. Some people are more susceptible to this influence however it is still not fully understood as to why. Scientists attribute this difference to the mutations in the gene.

To prove this point, Dr Jeff Barclay experimented with two identical worms with different mutations in their nervous gene. Both have undergone different mutational change. Both genes altered the way in which their nerve cells communicate and they had better alcohol tolerance than non-mutant worms.

Now that they have found a link between the gene and alcohol tolerance, they are also investigating whether the mutational gene can also combat the alcohol influence and ultimately reduce alcoholism in the society.

Jikyun Lee

s4161396@student.uq.edu.au

Surname Hidden Within DNA

2008-10-24T11:31:00.003+10:00

Dr Turi King of the University of Leicester’s Department of Genetics, the department that invented genetic fingerprinting, is developing another concept that could cause great advances in the field of forensics.

The link between a man’s Y chromosome and his surname has been the subject of Dr Turi King’s research. Her findings present the possibility that one day, after further research and development, a male’s surname may be predicted from his DNA alone.

In her research Dr King recruited over two and half thousand men with over 500 different surnames. In these men Dr King investigated the relationship between surname and Y chromosome type. She then went on to study 40 surnames in depth, recruiting many different men of the same surname but ensuring that known relatives were excluded from the study.

Given that like Y chromosomes, surnames are passed from father to son, Dr King has shown a link between surname and Y chromosome has the potential to connect all males with the same surname into one family tree.

Some cases showed that over 70% of men with a particular surname possessed similar or near identical Y chromosomes, whereas other, more common surnames displayed a number of different groups of related Y chromosomes within the surname.

This second effect is due to a particular surname having more than one founder and prevents the process from being so clear cut. For instance, the name Smith was derived from being a Blacksmith, so this name could have originated from a number of different men, resulting in a common surname having a group of different possible corresponding Y chromosome types.

At present there is a lot of development to be done on this discovery as there are many other factors that can influence surname. For instance, circumstances such as adoption and name changes would alter this genetic relationship.

If this area could be further researched, a database could be developed containing each surname with its related Y chromosome type/types. This would be revolutionary for the field of forensics, enabling identification, via surname prediction, of both the deceased and crime suspects.

Reference: University of Leicester (2008, October 8). DNA Could Reveal Your Surname. ScienceDaily. Retrieved October 24, 2008, from http://www.sciencedaily.com /releases/2008/10/081007192526.htm

Megan Steinberger (41767883)

Tiny Glimmer of Hope for Anencephalic Babies

2008-10-24T08:20:00.004+10:00

Anencephaly is a congenital birth defect, with approximately 1000 to 2000 anencephalic babies born each year in the United States. It is a neural tube defect characterized by a severe lack of brain development. If born alive, most anencephalic babies have a life expectancy ranging from just a few hours to a maximum of two days.

Anencephaly can sometimes be diagnosed through ultrasound, but unfortunately there is no genetic test and regrettably, no form of therapy or treatment. The underlying cause of anencephaly is still unclear and much disputed. However, researchers at the University of Illinois at Chicago have recently uncovered a possible clue as to why anencephaly occurs. Researchers created and attempted to breed mice that were missing the gene for the enzyme HSD17b7. Contrary to the expectations of the research team, the offspring died on the tenth day of gestation. The key observation in the experiment was that such mice exhibited the severe lack of brain development and deformities which are characteristic of anencephalic human babies. Although the exact gene that is missing or defective in human anencephaly is currently unknown, the fact the absence of the gene for the HSD17b7 enzyme causes the disorder in mice suggests that this same gene may play a role in humans. The brain is the most important site for HSD17b7 expression in the foetus, and this information further supports the idea that the absence of the gene for the HSD17b7 enzyme may result in anencephaly.

The researchers at UIC are now looking to test human anencephalic tissue for a mutation in the HSD17b7 gene. Conducting further study will hopefully open up pathways to greater understanding of anencephaly, and perhaps lead on to the development of genetic testing, and eventually, therapy to save precious new lives.

- Refaat

Article:
http://www.sciencedaily.com/releases/2008/10/081009162745.htm

Men’s Best Friend – In a New Way

2008-10-23T23:09:00.002+10:00

Dogs have been man’s best friends for centuries. Now, they have found a new way of impressing men- tracking down the genes and pathways involved in canine and human diseases via their genetic compositions.

It all started with two veterinarians, Gustavo Aguirre and Gregory Acland, initiating a project to understand the cause of inherited blindness in dogs 20years ago. They bred affected and unaffected dogs and tried to identify the inheritance patterns in the offspring. However, they came no closer to identify the genes. It proved to be too difficult for them at the time: geneticists had yet put numbers to canine chromosomes, and the human genome project had hardly started at that stage. This forced them to bank blood samples from their dog and wait.

The mapping of dog genome came a decade later. With their blood samples used as the raw materials, Gustavo Aguirre and his colleague’s long-sought-for gene, the gene for progressive rod-cone degeneration was finally found. This success, however, had given geneticists more than they had first sought after.

Geneticists have come to realize that dogs could be their dream model for genetic revolution. Dog breeders tend to keep their dogs as pure bred as possible. This means that they are often highly inbred for specific traits, and often their genealogies are well documented, which made the gene tracing easier – to track mutation across generations. Mutation from other species cannot simply enter the family without having them recorded in the genealogies.

So, what is it about with human? The close relationship of men and dogs actually means that they shared the same environment risk factor of having the same disease. Top 10 diseases in dogs include cancer, heart disease, epilepsy, allergies. Sounds familiar? They are the same top 10 diseases in humans. Consequently, geneticists think that dog genes might have the similar mutation that caused the diseases in human genes and they had turned to dog genome for clues.

With the dog genomes, you cannot trace too far back to find the mutations that cause a particular disease, the limiting factor is time of evolution – some inbred population exists only a few hundred years back. This is certainly better than tracing the human genome, where dozens of mutation can occur to cause the same disease. This certainly reduces the amount of samples needed to actually get the gene as shown by one of the geneticists that worked on dog genome. She used fewer than two dozen boxers to track down the gene for white coat color, the same mutated human genes that cause Waardenburg syndrome, which has the symptoms of hearing losses and pigmentation abnormalities.

At date, the progression of mapping dog genome for disease-causing genes is slow but with more and more geneticists starting to turn to dog genome, and more funding poured into the field, we will have more to expect in the future.

-Tze- (4155147)
Link: http://www.sciencemag.org.ezproxy.library.uq.edu.au/cgi/reprint/317/5845/1668.pdf

Newly Founded Role of 'Junk' DNA

2008-10-23T22:28:00.003+10:00

It had been founded 15 years ago that specific ‘junk’ DNA, also called repetitive sequences could transform into exons, which are parts of the DNA that code for a protein. Recently a University of Iowa found that certain 'junk' DNA evolved into exons play a role in gene regulation.

One type of repetitive sequences are called Alu repeats. Alu repeats are retrotransposons which undergo transcription to become RNA and then translate into DNA. Retrotransposons are a type of transposon. Transposons have the ability to cut themselves out of DNA and migrate to different areas in the genome.

Study's senior author Yi Xing, Ph.D., assistant professor of internal medicine and biomedical engineering has stated that Alu repeats are a major source of unique exons. Alu repeats are also specific in different primates which mean that exons produced in different primates will be unique.

A study was carried to determine the impact of exons in humans derived from Alu repeats. Researchers used a high density exon microarray. Scientists then analysed 330 of these exons in 11 human tissues. The team identified a number of exons with diverse and interesting expression. This allowed identifying exons that were likely to contribute to regulating gene expression.

One gene analysed which was SEPN1 which is involved in a type of muscle dystrophy. This gene was only expressed on greater levels in human muscle but not in any other human tissue or other species. This draws evidence that an exon derived from Alu is involved in regulating this gene in the muscle.

Access: http://www.sciencedaily.com/releases/2008/10/081017080145.htm

Genes responsible for weight problems

2008-10-23T21:52:00.005+10:00

By 41718867

Scientists, from Harvard school of Public Health in Cambridge, have recently found 2 molecules that they believe to be involved in the production of fat cells. They state that when a genetic mutation appears in one of these cells, either producing too many or too little fat cells, weight problems arise.

Furthermore, they also identified two other molecules, GATA-2 and GATA-3 that are believed to regulate how many fat cells are being produced. These molecules can either suppress the production of fat cells or up regulate them. It is believed that an error in this regulation could cause the fat cells to be overproduced.

The scientists concluded that because these molecules are expressed differently in each person, due to differences in genes, this can explain why some people have a tendency to gain weight while others can maintain a healthy weight throughout their life.

It is believed that once this is understood, we will be able to modify the body's ability to produce fat and therefore easily control of body's weight.

REFERENCE:

BBC NEWS, Genetic clues to obesity, http://news.bbc.co.uk/1/hi/health/958023.stm

LEDs May Help Reduce Skin Wrinkles

2008-10-23T12:47:00.000+10:00

Khoa Vu 41425996 BIOL1020 Blog Kerry P1

LEDs May Help Reduce Skin Wrinkles

Researchers in Germany conducted a study on reducing facial wrinkles by using high intensity visible light from light emitting diodes (LEDs). The study reports that high intensity light with a wavelength of 670 nm resulted in rejuvenated skin, reduced wrinkle levels and juvenile complexion when applied daily for several weeks. This treatment could be a future alternative to botox and cosmetic surgery for easing facial wrinkles.

The researchers also pointed out that high intensity visible light has been used for over 40 years to speed up healing of wounds. This means that light actually penetrates into the skin, causing changes in the sub-surface tissue.

They identified how the visible light works by changing the molecular structure of a glue-like layer of water on elastin, the protein that provides elasticity in skin, blood vessels, heart and other body structures. The light strips away those water molecules that are involved in the immobilization of elastin, gradually restoring its elastic function and thus reducing facial wrinkles. The researchers are confident that their approach can be easily converted to deep body rejuvenation programs.

Reference:

Sommer, A. P. & Zhu, D. 2008, ‘From microtornadoes to facial rejuvenation: implication of interfacial water layers’, Crystal Growth and Design, vol. -, no. -, pp. -.

Genetics blog - Patrick West

2008-10-23T11:34:00.000+10:00

Explaining The Body's Own Anti-HIV Drug

Humans have a built-in weapon against HIV, but until recently no one knew how to unlock its potential.

A study published online by the journal Nature reveals the atomic structure of this weapon - an enzyme known as APOBEC-3G - and suggests new directions for drug development.

APOBEC-3G is present in every human cell. It is capable of stopping HIV at the first step of replication, when the retrovirus transcribes its RNA into viral DNA.

The study's authors, led by Xiaojiang Chen of the University of Southern California, were able to show the atomic structure of the active portion of APOBEC-3G.

The discovery suggests how and where the enzyme binds to the viral DNA, mutating and destroying it.

"We understand how this enzyme can interact with DNA," said Chen, a professor of molecular and computational biology at USC. "This understanding provides a platform for designing anti-HIV drugs."

If APOBEC-3G works so well, why do people get AIDS? Because the HIV virus has evolved to encode the protein Vif, known as a "virulence factor," that blocks APOBEC-3G.

With APOBEC-3G out of the way, the RNA of the HIV virus can be successfully transcribed to viral DNA, an essential step for infection and for producing many more HIV viruses.

Chen said his group's research offers important clues on where Vif binds to APOBEC-3G. The knowledge could be used to design drugs that would prevent Vif from binding and allow APOBEC-3G to do its job, Chen said.

That would unlock humans' innate ability to fight HIV.

Are Soft Drinks worse than binge drinking?

2008-10-23T07:30:00.003+10:00

A health scare has erupted in recent years after a common preservative (211) has been found to alter DNA. Sodium Benzoate is a chemical produced naturally in berries and apples, but is used in large quantities by manufacturers to prolong the shelf life of soft drinks, sport drinks, cordial, biscuits, sauces and fruit juices. Sodium benzoate has proved a controversial additive, as recent studies have highlighted health concerns from its use.

Professor Piper’s research has found these chemicals to have the ability to cause severe damage to DNA in the mitochondria. Mitochondria consume oxygen to give energy and when damaged the cell starts to malfunction and can even be damaged to the point that they are inactivated. Diseases are being tied to damage to this DNA, including Parkinson’s, cirrhosis of the liver, ageing and potentially could be linked to a number of other neuro-degenerate diseases.

Oker-Blom (1981) studied the toxicology for the use of a modified sodium benzoate in treating arthrosclerosis of rats. Although effective in low doses, in doses above 30mg/kg there were detrimental side effects on the subjects. The subjects at low doses (10mg/kg) had acidophilic bodies and karyorrhexis present, indicating severely damaged liver cells and often died due to weight loss.
A review of sodium benzoate by the World Health Organisation and Food Safety Authority in 2000 found no evidence the additive was unsafe however more recent studies results are showing increasing trends towards the dangers of preservative 211. More research should be looked in the near future as the side effects on the liver and nervous system for the wellbeing of our society. We don’t allow school children to drink alcohol so why would we allow them to consume this preservative which has disastrous side effects on the body that not even continuous binge drinking could do to the body.

Trent Rogers 41403716

References
McCann D, Barrett A, Cooper A, Crumpler D, Dalen L, Grimshaw K, et al (2007). "Food additives and hyperactive behaviour in 3-year-old and 8/9 year-old children in the community a randomised, double-blinded, placebo-controlled trial" . The Lancet 370:1560-70
Oker-Blom, C. (1981) Toxicological studies on 4-(Hexadecylamino)Benzoate (PHB), agent with anti-atherosclorotic properties, in the rat. Toxicology Letters, 7, 273-277

How do changes in chromosome structure affect evolution?

2008-10-23T01:12:00.006+10:00

One important part of how new species form is that the new and old species can’t breed together.

One important part of sexual reproduction is having an even number of chromosomes. Whether each chromosome has a partner chromosome is crucial.

Whenever there are odd numbers of chromosomes or mismatched pieces, there will likely be mistakes during cell division. At the last step of meiosis, one chromosome from each pair moves into the new cells. An odd number of chromosomes means that one chromosome is left unpaired. It can go to either cell.

The end result is that cells end up with the wrong number of chromosomes. And this leads to sterility or birth defects.

Bananas are seedless becausethey have three of each of theirchromosomes.Let’s go back to the fact that apes have a split chromosome Two. And we have one big chromosome Two. The “split” chromosome Two in apes and our big chromosome Two would have problems sorting out where each chromosome should go.

The end result would be sterility or, more likely, miscarriage.For an everyday example, take the bananas you buy at the store. These bananas have 3 copies of each chromosome in their cells which makes them seedless. The bananas can’t make any seeds because they have an odd number of chromosomes.

During the cell divisions that make seeds, the unpartnered chromosomes cause all kinds of problems. As a result the seeds die. It’s likely that changes in chromosome numbers or structure are an important part of speciation. For a new species to develop there must be some reproductive barrier. This helps prevent interbreeding with the parent species. Some of those barriers could be changes in chromosome structure.

syahirah aqilah (s4188498)

Blame your parents for your sugar craving

2008-10-23T00:48:00.005+10:00

Have you ever wondered where your sugar craving comes from? It is a popular belief that smoking affects the sensitivity and preferences of sugary foods and drinks. A project was carried out by the Pennsylvania Department of Health to answer this question, with the suspicion that not only smoking, but the family history of drinking of alcohol may cause these cravings.

The project was carried out through an experiment on the effect of smoking and exposure to nicotine on the sweet taste sensitivity and preferences in women and a standardized questionnaire was carried on the subjects as well as the family members for any observations on the family history of alcohol and sugar craving. For testing of the sensitivity towards sweet tasting, a psychophysical method was taken place. The genetically determined sensitivity to the chemical called propylthiouracil (PROP) was tested, as previous research showed that PROP sensitivity is related to the sweet taste sensitivity. Already genetically inborn, the chemical ‘PROP’ can taste bitter to some people, while the others are not able to taste them or requires large amounts to feel the taste of it.

Overall, the results showed that more smoking reduces sucrose sensitivity and that the higher the family history of alcohol is, the more the subjects preferred higher sucrose concentrations and craved sweet foods often.

link to journal: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2268904

4159831

Telomere Dynamics and Longevity Gender Gap

2008-10-22T23:55:00.004+10:00

Telomere dynamics and Longevity Gender Gap

By: Anh-Thu Nghiem, 41092231

Telomere biology has just proved the Bible. Obviously, the Creator created humanity in two steps: a draft, which is Adam, and a ﬁnal, improved product - Eva. Eva is true diploid (XX) while Adam is in part haploid (XY, with Y is a much smaller chromosome). The facts that Eva has two X chromosome and Estrogen instead of Androgens lead to signiﬁcant biological advantages that might explain her better longevity.
Telomere (source: stemcells.
nih.gov/.../images/ﬁgurec2.jpg)

The linear eukaryotic DNA molecular suﬀers from the end-replication problem (Campbell & Reece, 2006) due to the inability of DNA polymerase to add nucleotides to 5’ end of the new strands in DNA replication. This problem causes DNA molecular to lose a number of base pairs every round of replication. Important genes are potentially eroded and ﬁnally lead to cell death. Eukaryotic cells ﬁx this problem by keeping long repetitive, non-coding sequeTelomere dynamics and Longevity Gender Gapnces (TTAGGG in human) called telomere at the end of the molecular to ensure that genes are not eroded away (Campbell & Reece, 2006). However, after many successive round of replication, telomere itself will be shorten. To ensure its protective eﬀect, it needs to be restored. Eukaryotic cells lengthen their telomere by telomerase. Telomerase adds repetitive sequence to the end of DNA using coding from a short RNA accompanying the enzym (Campbell & Reece, 2006). Unfortunately, telomerase presents in germ-line cells, but not in most soma cells. Consequently, erosion of telomere are associated with life-span of tissues and aging of the whole organism. In human, the rate of telomere erosion of white blood cells (WBCs) was found associated with(Aviv et al., 2005)
oxidative stresses (Cherkas et al., 2008).

It is an well-known fact that life expectancy at birth of women is some seven years longer than men (Aviv et al., 2005). It is called Longevity Gender Gap (LGG). Aviv et al., 2005 recommended interesting explanations of the phenomenon based on the interplay of somatic cell selection for X chromosome activation, estrogen activities and telomere dynamics.

Human telomere dynamics is often studied in WBCs. As expressed in WBCs, telomere length is highly heritable, inversely correlated with age, longer in adult women than men, and yet equivalent in newborn boys and girls. There are two factors that might explain the longer telomere observed in adult women: estrogen and somatic cell selection.

Estrogen’s eﬀects have two sides. Estrogen has a role in ameliorating oxidative stresses, which known to increase telomere erosion rate. As the same time, it stimulates the transcription of the gene encoding telomerase (Aviv et al., 2005). The eﬀects of estrogen on telomere dynamics may be attenuated or disappear altogether in older women, but its premenopausal inﬂuence could set telomere attrition at a trajectory that maintains longer telomeres in women throughout the entire human life span (Aviv et al., 2005).

There is good evidence for gene variance on the X chromosome that strongly inﬂuences telomere length. In normal female, one of X chromosome in somatic cells is stochastically inactivate during early embryo (no more than 25% of the gene in the inactive chromosome will be expressed). Newborn girls thus have two equal populations of somatic cells with respect to X inactivation (Aviv et al., 2005). Unbalance distribution of X inactivation develops later in life due to survival advantage of the ﬁtter between two types of somatic cells. More speciﬁcally, female cells in which a hypothetical ”short telomere allele” was
active would exhibit shorter telomeres at birth in comparison with those cells in which the active X chromosome carried a ”longer telomere” allele. As women age, their two somatic cell populations would become skewed toward the population that has comparatively longer telomeres, not only because telomere length appears to be inﬂuenced by an X-linked gene or genes but also for the reason that longer telomeres denote resistance to oxidative stress. Selection for cells with longer telomeres might produce greater tissue reserves and decreased mortality (Aviv et al., 2005). Calculating the rate of telomere
erosion and the mean telomere length in women and men show that disparity between the sexes is about 8 ”telomere years,” roughly the same as the observed gender gap in life expectancy (Aviv et al., 2005).

References

Aviv, A., Shay, J., Christensen, K., & Wright, W. 2005. Perspectives: The Longevity Gender Gap: are telomere the explanation? Sci. Aging Knowl. Environ, 23, DOI: 10.1126/sageke.2005.23.pe16.

Campbell, N.A., & Reece, J.B. 2006. Biology (Sixth Edition). Benjamin Cummings. Chap. 16. The molecular basis of inheritance, pages 287–302.

Cherkas, L.F., Hunkin, J.L., Bernet, S.K., Richards, J.B., Gardner, J.P., Surdulescu, Kimura, M., Lu, X, Spector, T.D., & Aviv, A. 2008. The association between physical activitiy in leisure time and Leukocyte Telomere Length. Arch Intern Med, 168(2), 154–158.

Evolution makes a species weaker ?

2008-10-22T23:28:00.001+10:00

There is a common misconception of the phrase "survival of fittest" as evolution always increases the chances of a species surviving. On the contrary, evolution sometimes reduces fitness of individuals or populations and may occasionally even lead to extinction through several ways.

There are 3 levels on which natural selection can act on – genes, individuals or populations. This does not suggest that what promotes the survival of a gene increases the fitness of the individuals carrying it. For instance, transposons who actually make their host organisms less fit are still capable of spreading through a population. These genes that could cause extinction of a population might have a practical use indeed. Biologists are now considering of releasing engineered transposons into populations of malaria-carrying mosquitoes.

Despite that, a population could be weakened through accumulation of detrimental mutations. Mutation is the essential source of supplying raw material for natural selection. If the mutation rate is too low a population will not be able to evolve fast enough to keep up with environmental changes. However, if it is too high, detrimental mutations may accumulate faster than natural selection can eliminate them. Eventually, the number of mutations can exceed the "error catastrophe threshold" which in the end causes the population to diminish. Nowadays, physicians wish to exploit mutation accumulation to treat diseases such as AIDS as HIV is already close to the error catastrophe threshold. Drugs that boost the mutation rate of the viruses to exceed the threshold might drive the population of viruses inside a person's body to extinction.

Furthermore, sexual selection could favour traits that decrease a species' overall fitness. One good example is the male peacocks with the biggest and brightest tails might attract the females, but lugging around a heavy, conspicuous tail would reduce their chances of survival. Studies of threatened bird species support the idea that sexual selection can indeed cause populations to extinct. It is actually surprising to find that features such as peacocks' tails evolve precisely because they are disadvantageous, compliant with the handicap principle. If an individual is trying to signal to females how fit and strong he is, that signal should be costly, such as growing a large, clumsy tail or giving away food so that there is no way for weaker males to cheat by making the same signal.

Anyhow, the author mentioned that the possibility of proving that any of these phenomena have ever led to extinctions is extremely small. This is because any species to which this has happened are, of course, no longer exist to study. However, the author believed that the indirect evidence is growing ever stronger.

Reference: Page, M L 2008, ‘Evolution myths: Evolution promotes the survival of species’, New Scientist, viewed 18 October 2008, http://www.newscientist.com.ezproxy.library.uq.edu.au/channel/life/dn13687-evolution-myths-evolution-promotes-the-survival-of-species.html.

Khai Chin Teoh (s4155084)

'Embryonic' Stem Cells From A Human Hair ! ! !

2008-10-22T22:55:00.000+10:00

By: Kim Nam Huynh

Embryonic stem cells collected from human embryos and used for cloning purposes have caused great debate on whether or not this process be adopted for the regeneration of damaged tissue/s in humans. Hence the field of research into alternatives for embryonic stem cells has revealed that hair cells can be used as an ‘embryonic’ stem cell substitute.

As we all know tissue cloning typical involves denucleating a totipotent cell (an oocyte) and nucleating it with one obtained from the patient. The purpose of using the patient’s nucleus is to transfer their genetic information to this totipotent cell. Once nucleated, this cell has the potential to differentiate into various forms of tissues found in the human body. The differentiated tissue/s will have the genetic information specific to that of the individual from which the nucleus was obtained.

Within the past decade, scientists have used similar mechanisms to alter the gene expression of a variety of cells found all over the body to be used as a substitute for embryonic stem cells. They include liver cells, intestinal cells, fibroblast etc. However, these cells are not totipotent and have restricted capabilities and cannot differentiate into all cell types found in the human body.

However, within the past week, scientific research in the Center of Regenerative Medicine in Barcelona, Spain have revealed that the modification of keratinocytes have provided scientist with patient-specific stem cells which are able to differentiate to any cell type found in the human body.

The vectors used to clone these cells are similar to the ones we used in module 2 involving the lacZ gene in cloning. Viral vectors are used to insert the genes for the master regulators: Oct4, Sox2, Klf4 and c-Myc into the kertatinocytes, this cell culture was allowed to proliferate. The matured cells are known as Keratinocyte-derived induced Pluripotent Stem Cells or KiPS cells.

Upon comparison of the KiPS cells with that of Fibroblast-derived iPS cells, the KiPS cells only took 10 days to form colonies whilst the Fibroblast-derived iPS cells took a typical 3-4 weeks. Another remarkable finding was that the success ratio of KiPS increased from 1~10 000 to 1~100 cells, meaning that these KiPS cells can be efficiently mass produced.

Hence the advantages of utilizing KiPS cells have aided scientists to mass produce totipotent stem cells potentially capable of regenerating vital cells and tissues in the human body. With the KiPS cell research, conditions such as Parkinson's disease can be treated at the neurotic level.

Autism: All in the Genes

2008-10-22T22:32:00.004+10:00

Claire Grant 41770744

Autism has long been misunderstood by the general public and even science. Society has long been confused as to how to interact with those who suffer autism, often affronted by their social hostility and inability to communicate. Given this reluctance, it has only been in recent years that research has been conducted looking into the cause of autism. Are autistics merely representative of their environment or is genetics the key to this condition?

Scientists and researchers at the School of Medicine in the United Kingdom have instigated an “Autism Genome Project”1, a preliminary investigation into identifying the gene/s responsible for autism. The project involved numerous scientists investigating 1200 families across an international forum. Families where multiple offspring suffered from autism were investigated using “gene chip technology”1.

The genome project looked specifically at the process of transcription and translation where base pair insertion and deletions are most susceptible to error. Scanning for “copy number variations (CNVs)”1 these base changes coupled with the research gathered from the “gene chip” investigation lead to the identification of a “previously unidentified region of chromosome 11 and neurexin 1” both widely believed to be involved in communication between neurons.

Neurexin 1 contains a specific set of neurons termed glutamates which if defective, scientists believe may affect the growth and development of these neurons and subsequently lead to developmental issues in the communication components of the brain.

The origin of conditions such as autism is paramount in deceasing prevalence of any condition and finding suitable intermediate relief of symptoms. Genetics is key in this improvement.

1. Green J., Lamb J. New insights into the genetics behind autism. [Online]. 2007. Available from: URL: http://www.medicine.manchester.ac.uk/aboutus/news/autismgenome

Isolation unnecessary in evolution

2008-10-22T19:26:00.000+10:00

It has been believed since the time of Darwin that isolation is necessary for evolution of a species, however this could be disproved through a study of cave-dwelling salamanders in Tennessee. The two main types of salamanders found in this area are surface-dwelling and cave-dwelling, which once interbred before they initially began to separate about 2 million years ago.

Such cave-dwelling salamanders were thought to be a classic example of isolation because as they continually evolved, they began to lose features such as eyes and pigmentation because they were unnecessary in their environment. However, many cave-dwelling salamanders have been found to show features that appear to be a hybrid of the two species.

To investigate this, DNA samples of both types of salamander were sequenced and after analysis, it was suggested that isolation was not the reason for losing unnecessary features. It was thought that gene flow still exists between the two species creating a hybrid; however natural selection appeared to be more dominant than gene flow between species.

It was then said by Andrew Hendry of McGill University that “speciation occurs in the face of gene flow much more often than many biologists are willing to admit.” This study could show that isolation is indeed not a necessary requirement for evolution, however more genetic analysis must first be conducted.

Holmes. B. Salamanders formed new species despite interbreeding. New Scientist. 25 April 2008.

Malaria Resistant Mosquitoes

2008-10-22T18:14:00.003+10:00

Malaria is an infectious disease passed on by an infective female Anopheles mosquito, which affects 300 million people a year, managing to kill over a million people annually. In sub-Saharan Africa, which suffers from 90% of all malaria cases, a child dies every 30 seconds from the infection. However, scientists have been researching into genetically modified mosquito’s that will contain a gene making them resistant to the malaria parasite, in turn decreasing prevalence and possibly eradicating malaria.
On release to the wild, this possibility exploits natural selection at its finest. Mosquito’s with the malaria resistant genotype will fare better in the environment than the mosquito’s that are able to be infected by malaria, which also compromises the health of mosquito’s. Experiments have been investigated, where the comparative genetic fitness of both the GM and wild-type mosquito have been tested. When both mosquitos were allowed to feed on malaria-infected blood the transgenic mosquito’s, after 9 generations, increased from 50% of the population to 70%. The results also showed that the mutated mosquito’s laid more eggs and had a greater rate of survival, hence making them more genetically fit in this situation. However, when the two populations were fed non-malaria infected blood, there was no change in allele frequency.

Although the results seem fairly positive, there are many more avenues which must be embarked on. This includes further research into newly proposed ideas, including the parasite’s ability to evolve and limit the success. Testing is crucial, and it has been suggested that the genetically modified mosquitos will not be able to be released into the wild for at least 10 years, providing that there is successful experimentation in the near future.

Referenced from: http://news.bbc.co.uk/2/hi/science/nature/6468381.stm

Genetic Differentiation In the World Today

2008-10-22T17:27:00.014+10:00

Millions of years have passed for the human genome to reach the point where it stands today in you and me, yet a group of researchers wanted to determine whether this highly specified genome of ours is still evolving. They set out to determine the degree of genetic differentiation in the world today by comparing the SNP genotyping of a variety of different ethnic populations2.

The SNP genotyping method provides a means of determining the genetic variation between members of the same species by analysing single base pair mutations, or single nucleotide polymorphisms (SNP), at a specific site on a chromosome, commonly referred to as loci1. When the first comparison was made between the genotypes of 60 European, 60 African, and 90 East-Asian individuals, the results proved that there was distinct evidence for genetic differentiation between these populations as a result of the genomic variation that has been evident around the world since the first of our species2. When further tests were carried out on the East-Asian sample population, differences in the SNP genotype of the 45 Chinese and 45 Japanese became evident. From undertaking this second test on the East-Asian sample population, the results also suggested that genetic differentiation was somewhat evident in subpopulations within Japan2. When testing this result it was determined that two distinct areas in Japan had differing SNP genotypic frequencies. The Ryukyu cluster, which accounts for the Okinawa region, was determined to have a higher frequency of the EDAR gene (T-allele) which is responsible for thick hair; and also the ABC11 gene (G-allele), responsible for ‘wet’ ear-wax, than its counterpart cluster, Hondo, which entails all the other regions in Japan (Hokkaido, Tohoku, Kanto-Koshinetsu, Tokai-Hokuriku, Kinki and Kyushu)2.

Evidence of genetic differentiation within populations today, is not only restricted to the Japanese, but research highlights that it is occurring at a similar level within the USA as well2. Our species will always be evolving, but in today’s society this evolution is not entirely essential to our survival, as we as a species have learnt how to manipulate the world to suit our needs, and developed the technology to allow “less-fit” individuals to survive long enough to reproduce and pass on their genes, that would otherwise not be desired if our survival was dependant on nature.

By Eva Blair (41793985)
http://www.sciencedirect.com.ezproxy.library.uq.edu.au/science?_ob=ArticleURL&_udi=B8JDD-4THTFB9-1&_user=331728&_coverDate=10%2F10%2F2008&_rdoc=4&_orig=browse&_srch=doc-info(%23toc%2343612%232008%23999169995%23699272%23FLA%23display%23Volume)&_cdi=43612&_sort=d&_docanchor=&_ct=17&_acct=C000016898&_version=1&_urlVersion=0&_userid=331728&_fmt=full&md5=5d5164c8c9a0773b3bcd0d93517f843d

Behind Enemy Lines

2008-10-22T16:30:00.002+10:00

Our immune systems are far from infallible. Most of us have suffered from a bacterial infection of some sort, whether it is the common cold or a sore throat. Others of us have had serious bacterial infections where we’ve had to be hospitalized. The treatment however is a quick round of antibiotics and we’re cured! So how would you feel, if your antibiotics failed and your condition worsened. The bacteria have gradually built up a resistance to the over-prescribed medication and nothing we know of can help you fight this new strain of microorganisms thriving in your body. This is the threat that medical practitioners are attempting to prevent at all costs.

Where we once thought that antibiotic resistance was our very own doing, Swedish researchers have discovered that it’s happening elsewhere too, somewhere that we’ve never been before, the arctic. A research team has uncovered a high degree of antibiotic resistance in arctic birds. Is it that these birds migrated over Southeast Asia and brought the resistant strains with them? Or has something far worse occurred… Has the bacteria developed a resistance completely on its own, without any modern medicinal connection, as a product of evolution? Whatever the reason, the implications are clear. A new age of “super bugs” is coming and we may be completely powerless to stop it.

By Prue Twiddle (s4178940)
Access at: http://www.sciencedaily.com/releases/2008/01/080111100636.htm

Genetics in the sporting arena

2008-10-22T15:44:00.002+10:00

What makes someone a better sportsperson than another? Could genetics influence our strength, speed or coordination? These simple questions have posed as a major issue in the field of genetics and in the sporting arena for some time. However; recently an allele – ACTN3 R577X – has been shown by researchers at the University of Maryland to influence the performance of elite-level strength athletes.

The genotype of the athletes and control group was determined through using restriction digest methods on the DNA obtained from whole blood samples. From these samples the consistency of the genetic trait was examined.

A study of approximately one thousand athletes from a variety of backgrounds and genders showed significantly lower X/X genotypes of the allele than a sample of the general public who were not athletes. Furthermore the allele appears to be a non-sense allele and thus it may be inferred that these athletes do in fact have a superior quality when compared to the general public. It was also shown through the use of the Hardy-Weinberg equation that those of Anglo-Saxon decent have a have a significantly lower frequency of the allele in comparison to the control group whereas those of ethnic race had no representation of the allele at all.
This discovery poses major implications for the world of sporting competition and research into such ‘mutations’. Although more research is definitely required; how can society use this discovery be used to assist the sporting arena rather than destroying it in the way performance enhancing drugs have done?

Reference:
Roth, S. M., Walsh, S., Liu, D., Metter, J. E., Ferrucci, L., & Hurley, B. F. (2008). The ACTN3 R577X nonsense allele is underrepresented in elite-level strength athletes. European Journal of Human Genetics , 391-394. http://www.nature.com/ejhg/journal/v16/n3/pdf/5201964a.pdf

s41714926

Logical bacteria: the way of the future?

2008-10-22T07:44:00.002+10:00

One of the newest genetic engineering tools are bacteria engineered to perform four logic operations: AND, OR, NAND and NOR. It is predicted that these logic units could be combined in different ways to engineer microbes “…with an internal decision tree logic” which would control their behaviors. The scientists hope that they would prove invaluable when designing microbes for uses such as fermenting biofuels or producing pharmaceuticals.

This is the first time logic gates have been introduced “for controlling gene expression in a living cell”, according to Kensaku Sakamoto of the Structural Biology Center in Yokohama in Japan.
At the California Institute of Technology in Pasadena, customised “snippets” of DNA were added to the tail of a gene, and that gene was then inserted into one of two types of cells – either E.coli bacterial cells or brewer’s yeast cells. As transcription of the DNA into RNA molecules occurred, these added snippets of DNA get entwined into twists of the RNA. These three-dimensional twists discern the presence of “input” molecules, and they react by either leaving the RNA alone or obliterating it into a true-or-false type of response.

Each snippet of DNA can have a completely independent design of the others, forming equally independent “twists” of RNA, which can be combined in different ways, making this destructive response occur from different logical input combinations.

As expected for the bacteria with binary logic, the California Institute of Pasasdena’s team used two types of inputs: tetracycline and theophylline molecules to create an AND or an OR gate.
In an AND gate, both molecules had to be attached to the RNA switch to prevent the destructive response from occurring, creating a green fluorescent protein “as an output”. In an OR gate, only one gate had to be open – meaning only one of the two molecules needed to be attached to create the output. A green output protein corresponded to a “true” result while destruction of the RNA and therefore the absence of protein signified a “false” result.

According to Christina Smolke of the California Institute of Technology, scientists are hoping for as much control over these bacterial logic circuits as engineers have over commonly used logic chips.

For more information, please visit: http://sciencenews.org/view/generic/id/37724/title/Bacteria_that_do_logic

Student number:41757905

Genes: Survival Secret of Antarctic ‘Antifreeze Fish’

2008-10-21T20:20:00.008+10:00

Five families of eight families of notothenioid fish, live in the icy waters of Antarctic continent. These fish can survive under temperatures that would turn most fish to ice. A study made in University of Illinois in 1960s discovered that some of notothenioids manufacture have their own “antifreeze proteins”, while these proteins bind to ice crystals in the blood to prevent the fish from freezing.

In a recent study, University of Illinois animal biology professor C.-H Christina Cheng and her colleges were the first ones aiming to try to understand the secret behind the genes that would eventually help to explain how the Antarctic notothenioids survive in such a harsh freezing environment.

The researchers wanted to know which genes were being expressed at high levels in Antarctic notothenioid Dissostichus mawsoni. Therefore, they analyzed gene expression in 4 tissues: the brain, liver, head kidney (the primary blood-forming organ in fish) and ovary of D. mawsoni. They found out that in each of these tissues, proteins were highly expressed from a small set of genes.

To get a better and deeper understanding, the researchers compared gene expression in D. mawsoni with the same tissues of unrelated, warm-water fish. And it was found that most of the genes that were highly expressed in the Antarctic fish were not found the same case in the warm-water fish.

And later on when they analyzed the upregulated genes, they found out that many of them coded for proteins that respond to environmental stress. There were many chaperone proteins, such as “heat shock proteins”, which protect other proteins from being damaged by stressed like extreme cold.

Other type of proteins called ubiquitins, were also found to be highly expressed in the Antarctic fish. This type of proteins help to maintain the health of cells and tissues by targeting damaged proteins for destruction.

At last, it was also found very high expression of genes coding for proteins that binds to reactive oxygen atoms or molecules in cells. These help the fish to avoid oxidative stress in the oxygen-rich Southern Ocean, as oxygen dissolves faster in cold water, and high levels of oxygen can produce highly reactive atoms or molecules that can damage cells and tissues.

The researches also compared gene frequency between the Antarctic fish to their warm-water cousins. And it was found that many of the genes that were highly expressed in the Antarctic fish were present in three-to-300-fold more often then in their warm-water cousins.

However, researches are still continuing in order to understand how global climate changes would affect the Antarctic fish.

(Student no.: 41596627)

Reference
Chen et al. Transcriptomic and genomic evolution under constant cold in Antarctic notothenioid fish. Proceedings of the National Academy of Sciences, 2008; 105 (35): 12944 DOI: 10.1073/pnas.0802432105

From: Science Daily

http://www.sciencedaily.com/releases/2008/10/081016124049.htm

Circadian clock does more besides than guiding our daily cycle

2008-10-21T19:23:00.006+10:00

In humans and other mammals the primary body clock is located in the suprachiasmatic nuclei, a cluster of around 10 000 neuronslocated on either side of the mid line above the optic chiasma,about 3 cm behind the eyes. According to Stanford researchers, the circadian rhythm that quietly pulses inside us all, guiding our daily cycle from sleep to wakefulness and back to sleep again, may be doing much more than just that simple metronomic task. Working with Siberian hamster, researchers found that without the functioning of circadian system, they are unable to remember what they have learned and it obstructs their learning process. In addition, it gets even more sleep than usual without the circadian system. Although they are getting loads of sleep, these animals still performed terribly on a simple learning task.

The change in learning retention appears to hinge on the amount of a neurochemical called GABA, which acts to inhibit brain activity. The circadian clock controls the daily cycle of sleep and wakefulness by inhibiting different parts of the brain by releasing GABA. If the hippocampus (the part of the brain where memories are stored) is overly inhibited, then the circuits responsible for memory storage don't function properly.To test that idea, researchers gave the circadian-deficient hamsters a GABA antagonist called pentylenetetrazole (PTZ), which blocks GABA from binding to synapses, thereby allowing the synapses to continue firing and keeping the brain in a more excited state. It is successful where those learning-impaired hamsters caught up with their intact peers to exhibit the same level of learning retention.

This finding has implications for diseases that include problems with learning or memory deficits, such as Down syndrome or Alzheimer's disease. Research on people with Down syndrome has shown that one reason they don't perform well on cognitive tests is that they grow up with what amounts to an over-inhibited brain. Studies on mice that exhibit symptoms of Down syndrome have demonstrated that when given PTZ, the mice demonstrate improved learning and memory. Besides that, aging of humans is one of the big things that happens in the circadian system that starts to degrade and break down. The degradation of circadian rhythms in elderly people may contribute to their short-term memory problems.

What this says is that the circadian system is necessary for something that is deeply important: learning.

Melissa Hum Wen Ching~41796856

Sources:
1) http://www.sciencedaily.com/releases/2008/10/081008151318.htm
2)http://www.bmj.com/cgi/content/full/317/7174/1704

Gene Linked To Commitment-Phobia

2008-10-20T22:34:00.001+10:00

Men with a common gene variation for "bonding" hormone report more marital strife

A particular gene variant seems to predispose men to relationship issues.Graphic: A. Nandy / Source: Walum, et al.

There’s news for women who want a man who bonds instead of a James Bond: Scientists have identified a common genetic variation that appears to weaken a man’s ability to emotionally attach to one partner.

The study, to appear in the Proceedings of the National Academy of Sciences, is the first to try to examine whether a hormone that encourages monogamy in animals plays a similar role in male humans. Before getting ideas about a DNA-fidelity test, though, women should consider that the study wasn’t designed to determine how much — or even whether — the gene in question is responsible for monogamy in humans.

“We can’t with any accuracy predict effects on behavior,” says Hasse Walum of the Karolinska Institute in Stockholm. “A lot of different things determine how happy you will be in a relationship.”

But women can now wonder, “What about his vasopressin 1a receptor subtype?”

The hormone vasopressin affects several body systems, including cardiac and urinary function. In addition, scientists have long studied how vasopressin influences behavior in prairie voles. The mouselike animals, found in the grasslands of North America, are famous for social monogamy. Males tend to be family guys, sticking close to home and helping to raise the pups. Even related species such as meadow voles don’t bond for so much as a romantic weekend.

Over years of study, scientists have concluded that prairie vole bonding has much to do with vasopressin activity in the brains of males. Through a series of studies that manipulated vasopressin levels in the vole brain, scientists have even made the animals more, or less, faithful. Vasopressin is not a love potion, though. Nerve cells also have to be equipped with specific receptor molecules that allow the hormone to bind to the cell and activate certain internal circuitry.

The new study examined a gene that codes for a vasopressin receptor in the human brain. In addition, Walum and an international team of collaborators also had volunteers fill out questionnaires to measure their level of “pair bonding” and marital strife. About 500 couples, who had been together at least five years, answered questions such as, “How often do you kiss your mate?” Or, “Have you discussed divorce or separation with a close friend?”

In the end, one particular variation of the gene, called allele 334, was associated with lower scores on partner bonding and greater odds of marital conflict. The effect was concentrated in men. For instance, among men either with no copies or just one copy of the 334 allele, 15 to 16 percent reported a marital crisis in the past year. However, when men had two copies of the 334 allele, the odds of marital crisis doubled, to 34 percent.

“I think this is actually a real breakthrough paper,” says Steve Phelps of the University of Florida in Gainesville. “The magnitude of effect is really astonishing.” He says that few studies of behavior find large effects for single genes.

But he and others were also cautious. “I think the results are really intriguing,” says Larry Young of Emory University School of Medicine in Atlanta, who in 2005 reported in the journal Science that a variation of the same gene predicted the quality of bonding in male voles. “I still remain skeptical until this can be replicated,” he says.

And even if the association holds up in further experiments, it doesn’t mean that women would want a future husband to submit a genetic sample for allele-334 testing, Young says. Marital harmony is determined by the behavior of two complex individuals, of which genes play only a part.

“It will be labeling a lot of people in a way that will be absolutely wrong,” Young says. “There’s so much more that goes into the quality of a relationship than a single gene.”

Gene linked to commitment-phobia

By Laura Beil

September 27th, 2008; Vol.174 #7

http://www.sciencenews.org/view/generic/id/36069/title/Gene_linked_to_commitment-phobia

Genetic predisposition towards alcoholism

2008-10-20T20:32:00.001+10:00

Alcoholism is a disease in which sufferers develop dependence on alcohol; which can lead to many negative consequences: economic, social and physiological. Evidence of genetic linkage has been established to this disease. Another factor which leads towards this disease is environmental (as the disease requires the consumption of alcohol in the first place in order for it to manifest). It is the pharmacokinetics of ethanol metabolism that influences the risk for alcohol dependence.

There are two metabolic pathways for ethanol metabolism, involving oxidation to acetaldehyde (catalysed by alcohol dehydrogenases, ADHs); and followed by further oxidation to acetate (catalysed by aldehyde dehydrogenases, ALDHs).

Studies were conducted on families in which at least 3 members were diagnosed alcoholics; which showed evidence that the risk of alcoholism is linked to a broad region on chromosome 4q. The genotypes of single nucleotide polymorphisms (SNP) across the ADH genes were analysed. Humans have seven ADH genes (tightly clustered on chromosome 4q22). Variations encoding for three alcohol metabolizing genes, ADH1B, ADH1C, ALDH2 and ADH4, are associated with the risk for alcoholism. The high risk alleles are the variations which have lower activity. A variation of one of these alleles (commonly found in individuals of Asian descent) has been shown to be protective against alcoholism; whereas a different allele has been linked with binge drinking and alcoholism in Native American populations; and a further variation (commonly found in individuals of African ancestry) metabolises alcohol at a higher rate. Another study that was conducted also found that along with alcoholism, there is also a link between certain ADH4 gene variations and cocaine dependence.

Many studies have shown clear evidence of the genetic link between alcohol dependence and the genes found on chromosome 4q; meaning that some individuals are genetically predisposed towards suffering from alcoholism; and individuals of different ancestry can be affected by alcohol in very different ways.

Original article:
Association of alcohol dehydrogenase genes with alcohol dependence: a comprehensive analysis: http://hmg.oxfordjournals.org/cgi/reprint/15/9/1539

Of the things that bacteria do... housekeeping?

2008-10-19T19:55:00.007+10:00

From the depths of a flooded mine, scientists from several American institutions have discovered a world in which bacteria are found to emit proteins that sweep up metal nanoparticles into immobile clumps.

The research has revealed that the bacteria actually secrete the proteins out into the environment. These proteins then travel far from the microbe that produced them, and then amass metal nanoparticles into clumps that are too large to be swept away be underground currents. How and why the bacteria carry out this bit of housekeeping remains a mystery, but this novel discovery may lead to new ways of bioremediation methods designed to trap harmful metals such as Uranium, Arsenic and Plutonium.

The research team analyzed a biofilm rich in sulfide metabolic waste product of the bacteria that thrive in the oxygen-free mine. Once the sulfide is released by the microbes into the watery environment, it readily combines with metals, in this case zinc, to form nano-sized biominerals that measure about one-billionth of a meter in diameter.

When analysed under a transmission electron microscope, they found that the zinc sulfide nanoparticles were arranged in dense aggregates. The question asked now is: Why do the nanoparticles group together? Something so small should disperse throughout the mine. Instead, the metal nanoparticles form blobs that measure several microns in diameter, and these larger blobs anchor the nanoparticles in place. Stopping nanoparticles in their tracks, as this process does, could become a critical component of a bioremediation strategy.

The team further analyzed the zinc sulfide aggregates and detected the characteristic signal of proteins. They found proteins and polypeptides embedded within the zinc sulfide nanoparticles. Specifically, the nanoparticles were arranged like tree rings, and the proteins coated the particles’ surfaces and filled the gaps between them.

But why do the bacteria go through the trouble to do this? Perhaps the bacteria use the protein to sequester their sulfide waste product, which could otherwise accumulate and entomb the bacteria or interfere with their cellular machinery. Or the process could have actually occurred the other way round: Proteins and peptides could be released by bacteria after they die, and are then scavenged by zinc sulfide. Simply put, no one knows. Regardless, the process stops the spread of metal nanoparticles in natural environments, which is reason enough to explore it further.

YunKit - 41810912

Reference:
Extracellular Proteins Limit the Dispersal of Biogenic Nanoparticles
John W. Moreau, Peter K. Weber, Michael C. Martin, Benjamin Gilbert, Ian D. Hutcheon, and Jillian F. Banfield
Science 15 June 2007 316: 1600-1603

Yin and yang of genes at play

2008-10-19T14:42:00.004+10:00

We have always thought that environmental stressor is a major cause of mood disorder. However, studies show that the probabilities of having depression can be contributed not only by the environment but also by the heritable traits in the master molecule of life, the genes. There are two genes that work hand in hand for making your nerve-racking day much more miserable.

The gene that code serotonin transporter protein has been shown to increase the risk of depression in the context of stressful life events. There are a number of studies that revealed people with one form of this gene called SLC6A4 have risk up to four times greater to having depression. This form of gene influences the impact on the development of a system in the brain relating to how environment is experienced emotionally.

Besides that there is another gene called BDNF that regulate the expression of a protein that play a vital role for allowing serotonin gene to cause these development effects. Fascinatingly, the BDNF gene is also the risk factor that caused mood disorder. Hence, the basic molecular link between SLC6A4 and BDNF is a critical interaction that would impact on the development of emotion regulation system in the brain.

These studies concluded that the reliance characteristic of SLC6A4 against BDFN can give either positive or negative impact to the brain system depending on the form of BDFN gene. In a nutshell, the risk of mood disorder is based on the combinatorial effects of interacting risk factors from these two.

Source: http://www.sciencedaily.com /releases/2008/03/080312172620.htm

Siti Zulkifli (41617205)

The stinging root of jellyfish

2008-10-18T19:05:00.003+10:00

Ever wonder how jellyfish got its sting?

Recently discovered similarity between one of the gene required for them to sting and a bacteria gene led scientists to believe that ancestors of jellyfish obtained the gene from the microbes. In jellyfish, this gene codes for a subunit of poly-gamma-glutamate (PGA) synthase where PGA is a major component of stinging cells. PGA collects positive ions, allowing cells to regulate its osmotic pressure. This results in the unleashing of the poisonous barb when there is sudden change in pressure. The same compound forms the protective capsule in bacteria. Appalled or not, PGA is also responsible for the stringy texture and strong smell of fermented Japanese food natto.

Nicolas Rabet of the Pierre and Marie Curie University believes that the gene is transferred via horizontal gene transfer, although for most of the time, this type of transfer is deemed unimportant. By phylogenetic analysis, Rabet and his team not only found that the gene in jellyfish fits well in the bacterial family, this gene has also being picked up by certain, sponges, worms and fungi. Although some scientists do not agree, others are now finding that horizontal gene transfer is not so uncommon in the animal world they first thought.

All in all, mankind will never cease to be amaze as to how small creatures like bacteria have so much influence in nature.

Original article: Dance, A. (2008, September 28). How the jellyfish got its sting. Nature, http://www.nature.com.ezproxy.library.uq.edu.au/news/2008/080928/full/news.2008.1134.html

Han Siean Lee (41617009)

Life Saving APOBEC-3G

2008-10-18T15:19:00.001+10:00

Human immunodeficiency virus (HIV) is a virus that weakens the immune system in humans. It is found in the blood, semen, and vaginal fluid of a person who has HIV. It can lead to acquired immunodeficiency syndrome (AIDS), a condition in humans in which the immune system begins to fail, leading to life-threatening opportunistic infections.

For most people who have HIV, the progression to AIDS is fairly slow, taking years from HIV infection to the development of AIDS. Without treatment people who have HIV eventually become ill and can develop AIDS within five to ten years. However there are a small percentage of people who do not show any deterioration in their health, even after ten years.

Every human being has the enzyme APOBEC-3G, it has the ability to fight against HIV. The way this enzyme work is by stopping HIV at the first step of replication, when the retrovirus transcribes its RNA into viral DNA. Xiao Jian Chen from University of Southern California discovered the structure of the active portion of APOBEC-3G, and showed where the enzyme binds to the viral DNA, how it mutates and destroys it. The discovery of this enzyme developed a new path for HIV treatment.

By now you might be wondering why people still get AIDs when they have APOBEC-3G in their bodies. This is because HIV encodes the protein called virulence factor (Vif), which blocks APOBEC-3G. Without APOBEC-3G, the RNA of the HIV virus can transcribe to viral DNA and produce more HIV viruses.

This significant discovery gives new hope to researcher and HIV patients. If the method of preventing virulence factor from blocking AOBEC-3G enzyme is known, many unfortunate lives can be saved.

Source: http://www.sciencedaily.com/releases/2008/10/081012164445.htm

Yes, blame it on the genes

2008-10-18T01:56:00.005+10:00

Ever wonder why the obese are, well, obese? New research has shown that the ‘culprit’ is a neurotransmitter called dopamine.

When we eat, the brain releases the pleasure-inducing chemical dopamine. However, the gene Taq1A1 reduces the number of dopamine D2 receptors, hence slows down the effect of dopamine. In order to compensate with this deficiency, those with this gene eat more. This suggests that people with the gene Taq1A1 are more vulnerable to obesity as compared to those without.

Tests on 53 female university students and 33 teenage girls were done to monitor the activity in the dorsal striatum in female brains as they consumed chocolate milkshake and a tasteless solution. It was found that it if the activity in the brain’s dorsal striatum is slower, the chances of the participant to gain weight are higher.

To prevent this, Dr Eric Stice, a psychologist at Oregon Research Institute proposed that people with a lower number of dopamine receptors should consume more rewarding substances to go through the same level of pleasure as others.

41617193

Reference:

http://www.cbc.ca/health/story/2008/10/16/food-brain.html
http://www.medicalnewstoday.com/articles/125778.php
http://www.wtopnews.com/?nid=106&sid=1498449

Jaws without a father?

2008-10-17T11:10:00.004+10:00

To this date, the greatest predators of nature have been known as lonely, single creatures that hunt and live alone. However, a recent discovery by Dr. Damien Chapman just about confirms that sharks do not mind their solitary lifestyle. Or at least the female ones don't.

I don't think it has come to anyone's mind that a female shark could actually reproduce without a partner. Yet. However, for just the second-time-ever, a female shark has reproduced without the need of a male shark sperm. This trait shocked the science world back in May 2007 when a hammerhead in Nebraska Zoo somehow managed to reproduce despite being isolated from its male counterpart for at least 3 years. Only one year later, a female blacktip shark managed to do exactly the same. When DNA testing confirmed that these were virgin births (known as parthenogenesis) scientists were left clueless about how this could have occurred.

However, the second coming of this phenomenon seems to have filled some gaps that had many scientists speechless. For one, Dr. Chapman believes that these unusual behaviours of the female shark weren't just a freak show, in fact, he believes that parthenogenesis is something that occurs in many different species of sharks, and that it was a phenomenon that could most likely be observed occasionally, and that it wasn't a once in a blue moon sort of thing.

Another discovery that Chapman noted was that in the case these virgin births occur, only one offspring is produced, whereas in normal reproduction, a female shark usually gives brith to a few to a hundred pups. He also noted that during shark parthenogenesis, the offspring receives only one set of chromosomes - from the mother, that becomes paired with an identical set of chromosomes, again from the mother. This bizzare characteristic could only mean that there was no father, and that the heritable traits were from a single source.

Parthenogenesis has only been confirmed in some bony fish, amphibians, reptiles and birds. However, through a more advanced study in genetics sharks have been added to this exclusive list. It has caught Dr. Chapman's as well as my attention that maybe this could be the key to combatting extinction of some rare shark species that have become a common target to fishermen. Only time will tell if parthenogenesis is the key to combatting extinction.

By Terry Hong
41720002

Reference:Chapman et al. Parthenogenesis in a large-bodied requiem shark, the blacktip Carcharhinus limbatus. Journal of Fish Biology, 2008; 73 (6): 1473
Article at Science daily :'Virgin Birth' By Shark Confirmed: Second Case Ever
URL:http://www.sciencedaily.com/releases/2008/10/081010173054.htm

Only a Mother Could Love?

2008-10-17T01:11:00.002+10:00

Just looking once at the platypus should give you an idea of why the animal has caused so much controversy in the zoological world. Is it a mammal with a duck beak? A reptile with fur? Or a UQ zoology experiment gone terribly wrong? The recent sequencing of the platypus genome sought to bring forth an answer to these rather perplexing questions.

The sequencing libraries were prepared from DNA of a single female platypus, and the DNA sequences in this library were used to define the protein-coding gene content of the platypus, as well as look to find any genetic similarities with marsupials, reptiles, or mammals. The researchers found that majority of the platypus gene, 82%, were orthologues, genes that have remained as single copies without duplication or deletion in platypus, Eutheria and in Opossum. Further analysis of the platypus’ genome found that the platypus had retained a single vitellogenin gene (vitellogenin is an egg yolk precursor protein), while on the other hand, sauropsids such as the chicken have three, and viviparous marsupials and eutherians have none - suggesting that the platypus is an amazing halfway-point between the two.

The platypus chromosomes, like the animal, are also a little strange. The animal has 52 chromosomes, including 10 sex chromosomes - quite unusual when compared with other mammals. The researchers also compared specific platypus genes to chicken and human genes, and found that the creature, having more in common with chicken Z chromosomes, probably evolved directly from a bird-like ancestral reptilian system.

Finally, the genes and gene position of genes deciding lactation and dentition in the platypus are quite similar to mammalian genes. Platypus casein genes, which play a major role in lactation, are tightly clustered together in the genome like in other mammals, and adjacent to these genes, like in mammals, are tooth enamel matrix protein genes, even though adult platypuses lack teeth!

This research may help us better classify the platypus in terms of class, but it also broadens our biological understanding– the mixture of reptilian, mammalian and unique characteristics of the platypus genome will hopefully provide many clues to the function and evolution of all mammalian genomes.

Source:

Washington University School of Medicine (2008, May 7). Platypus Genome Explains Animal's Peculiar Features; Holds Clues To Evolution Of Mammals. ScienceDaily.

URL: http://www.sciencedaily.com /releases/2008/05/080507131453.htm (Accessed 16^th/10/08)

By Damir Krehula

Trace your roots!

2008-10-16T22:58:00.001+10:00

Interested to discover your ancestors and know where they come from? Have a go with DNA Ancestry Project. This new exciting project developed by GeneBase BioNet is helping people in tracing their ancestral origins from thousands years way back. Studies have shown that our common ancestor was originated from Africa approximately 65,000 years ago. From that time, our ancestors have scattered out into the Middle East, Asia, Europe, North America and other parts of the world. Throughout time, mutations occurred naturally in their DNA and each mutation specifically linked our ancestors to time and place in history. These mutations are important as they allow us to trace our distant ancestral lines. So, it is highly possible for us to discover our family history through genetic genealogy.

Starting the participation in this project is easy; you just have to choose either to trace your paternal or maternal line and then send your DNA sample to their lab where they can find out the percentage match of your marker to markers around the world. Some famous DNA that have been analysed were from Genghis Khan, Thomas Jefferson (third US president) and also The Romanovs (the last imperial dynasty of Russia). Who knows you actually ties to royalty and legendary figures!

Reference:

http://www.dnaancestryproject.com/index.php

By:

Nurul Aina Mohamad

41550638

Insomniac fruit flies

2008-10-16T20:38:00.004+10:00

Sleep has been a very important routine in lives that we spent a third of our lives on it. Since there is so much time spends on sleeping, several researches have been done to identify the specific gene that causes us to sleep.

Although the gene is not identified yet in human, a group of researches from University of Pennsylvania School of Medicine have identified a gene that responsible in controlling sleep in fruit flies. When studying on 3500 fruit flies, the team had discovered mutants that can live with lack of sleep or even did not sleep at all. These flies have a mutation on their gene, named sleepless gene.

This sleepless gene encodes a protein that affects the opening and closing of potassium ion channels in the brain. If the channels are opened, the brain will be working and the flies will be awake. But if the channels are closed, the brain will not be connected and not working, hence causing the flies to sleep. Mutant fruit flies are lacking of this sleepless-produced protein. Therefore, these mutant fruit flies will only sleep for one or two hours a day or none at all.

However, little sleep has affects the quality of life of these mutant fruit flies. They have shorter life span, where they only live half as long as normal fruit flies. Besides, they also have problems with their coordination and restlessness.

Perhaps, if human sleep gene can be isolated in future, we will understand better of human sleep and also find a treatment for sleeping related problems such as insomnia.

Source: http://www.sciencedaily.com/releases/2008/07/080729160819.htm

41551701

Are you fat? Do you have an irresistible urge for Hungry Jack's? Put 1 and 1 together but you don't get just 2.

2008-10-16T20:11:00.001+10:00

A Human adenovirus-36 & a Burger(!)

Yes, you probably do; so do I.

Apart from its great taste, why else would anyone grab a Whopper double beef with cheese *drool* that is filled with *ahem* 65.1 grammes of fat (100% daily value), of which 25.1g is saturated (126% daily value)?
Don't you want to stop all this madness, stop all the fats from entering your body, stop your weight shooting for the sky, stop Hungry jack's from taking over your life?
Sadly, that's what YOU want, but not YOUR body. Nature has its own way of logic. It does not care how you look or how unsightly your belly is, your body sees fat as its great pal.

The body is an efficient piece of work, and it is engineered to put your survival as its utmost importance. You can say that it will do almost anything to keep you alive (That sounds very selfish).
As you know it, fat is the richest source of nutritional energy at 37 kilojoules per gramme. It's no wonder the body likes fat, it provides energy with so little input. Fat is biologically favoured whether you like it or not.
Scientists have suggested that fat intake is triggered by the neuropeptide galanin. This protein when secreted causes the person to crave for fat, and offers an explanation as to why when we are hungry, we are likely to crave fat.

So, the interesting fact is, that your love for Hungry Jack's is partially accounted for by your genes (not forgetting the great taste). The GAL gene (whose expressed product codes for galanin) is located on chromosome 11 in humans. The galanin protein is a chain of 30 amino acids.

But this does not mean you can put the blame of your belly fat solely on your genes.
As I've mentioned in the title, your craving for Hungry jack's + your fat = not 2. There's something else playing hard to get.

Some time in 2007, a bunch of scientists from Boston have reported new evidence that a common viral infection can cause obesity in humans *gasp*. Laboratory experiments have shown that infection with human adenovirus-36 (Ad-36) transforms adult stem cells obtained from fat tissue into fat cells. As a control, stem cells not exposed to the virus were unchanged.
Another bunch of scientists have identified a gene - E4Orfl, in the Ad-36 virus that appears to be involved in causing fat accumulation observed in infected animals (in the experiment).

Despite the odds...
To all Hungry Jack lovers: Be warned!
To all of you wanting to lose weight: You're not alone.
To all of you reading this: stay healthy. :)

kit - 41810912

Reference:
http://www.positivepath.net/ideasMC5.asp
http://www.eurekalert.org/pub_releases/2007-08/acs-cvm081007.php
http://caloriecount.about.com/calories-hungry-jacks-whopper-double-beef-i94616
http://en.wikipedia.org/wiki/Galanin

No Learning without the right Rhythm

2008-10-16T13:01:00.001+10:00

An experiment with Siberian hamsters has shown that they can’t remember anything if their circadian clock doesn’t function. The circadian rhythm is a roughly-24-hour cycle in the biochemical, physiological or behavioural processes of living beings. It is genetically encoded and external clues (so-called ‘Zeitgeber’) help in synchronizing the circadian clock. Until now, it had not been shown that the circadian clock is crucial to remembering and learning. Biologist Norman Ruby and his colleagues applied a technique which completely disabled the circadian system of the Siberian hamsters. The circadian clock controls the daily cycle by releasing the neurochemical GABA into different regions of the brain during the day. GABA inhibits brain activity and if the hippocampus (part of brain where memories are stored) is overly inhibit it has a negative effect on learning as these regions need to be excited in order to retain information and encode it at a molecular level. The circadian-deficient hamsters were confronted with a simple test called a novel recognition task. The hamster was put into box in which the researchers had placed 2 identical objects (e.g. 2 shot glasses) in adjacent corners. The hamster will then go and explore these two objects, spending approximately equal amounts of time on both objects as both are new to the hamster. After 5 minutes the hamster is removed from the box and one of the objects is replaced with a very different one. When faced with the old (known) and new (unknown) objects the animal would under normal circumstances dedicate most of its time exploring the new object. In the experiment though the hamster still spends equal amounts of time on exploring the old and the new object. This means that the hamster doesn’t remember it has explored the old object already. To confirm this was due to the GABA level (and thus disturbed circadian rhythm) the hamsters were then given an antagonist which blocks GABA from binding to the synapses. These hamsters were able to keep up with hamsters with normal circadian function. The results of the experiment have implications for diseases including learning difficulties and memory loss such as Down Syndrome and Alzheimer. Down Syndrome causes parts of the brain to be over-inhibited due to high GABA levels, and mice which were fed the antagonist improved their learning. In aging humans one of the most important changes when aging is the breakdown of the circadian clock (sleeplessness, confusion as to which time of the day it is). This results in high GABA levels resulting in information not being stored in the brain. The results of this research may lead to new approaches in treating Alzheimer and learning deficiency diseases.

http://www.scientistlive.com/lab/?/Medical/2008/10/09/21147/Circadian_clock_and_remembering

Anna Rada
41855137

Gene manipulation to produce Fluorescent Cats

2008-10-16T10:22:00.004+10:00

Scientists have added a fluorescence protein to the DNA of three cats and then cloned them, to find that their offspring glow a dull red under ultra-violet light. The experiment, successfully carried out in December 2007 by a team of South Korean Scientists from Gyeongsang National University, took skin cells from 3 female cats and used a virus to insert the instructions to produce the red fluorescence protein. They then took the gene-altered nuclei and inserted them in an egg for cloning. These modified eggs were then implanted back into the cats they came from, turning them into surrogate mothers for their own clones.

The huge implications for this breakthrough lie in the fact that if you can insert instructions into DNA to cause skin to fluoresce in cats, then theoretically you should be able to insert other things into other animals. Humans could be cloned with DNA instructed as to what hair colour they should be born with, what body type they should have, or even what diseases they would or would not be prone to. This type of experimentation is not likely to happen very soon though, as human experimentation with cloning is illegal throughout the world.

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References

http://www.koreatimes.co.kr/www/news/biz/2007/12/123_15447.html

Earth's Lonliest Bug? by Lynne Baillie 41822090

2008-10-16T08:33:00.008+10:00

A bacteria has been discovered 2.8km inside the Mponeng African goldmine, and is thought to hold the key to Alien life. The organism has never been exposed to light or oxygen in its 60 C heat atmosphere.

Dylan Chivian of the Lawerence Berkeley National Laboratory, CA, has examined the DNA present and confirmed that 99.9% of the genetic material belongs to Candidatus Desulforudis audaxviator; a single bacteria in a single ecosystem.

The thing that's confusing scientists is that is is unheard of for a single species community in the microbial world. This organism has everything it needs in its genome to survive in a virtually dead environment within the rock.

D.audaxviator is shown to get its energy from the radioactive decay of Uranium in the surrounding rocks; and has genes which give the ability to extract carbon and fix nbitrogen from its environment.

Chris McKay, of NASA's Ames Research Centre is intrigued by the discovery. He believes this is proof that life in one organism can be entirely self-sufficient without any prior involvement of the sun, and without an oxygenated environment- perhaps something which could occur somewhere else in the Universe?

The bacteria is thought to have got there via travelling through the rock and using horizontal gene transfer, a type of genetic engineering, to inherit some of the archaea genes. The water the bacterium was found in was estimated at 3 Mya, perhaps giving an indication of the age of the organism and rationalising its inability to survive in an oxygenated environment.

The discovery certainly has people talking, with some discussing DNA for fixing nitrogens applications as a fertiliser to reduce pollution if inserted into crops. Mars and Saturn's moon Enceladus are also being studied as candidate planets for a bacteria like this to evolve in. Both of these planets have shown the presence of water, and Mars in particular is highly radioactive.

The discovery marks a turning point in our knowledge of the microbial world and in the possibilities of life forms on other planets.

References
http://environment.newscientist.com/article/dn14906-goldmine-bug-dna-may-be-key-to-alien-life.html
http://www.space.com/scienceastronomy/solarsystem/mars_radiation_020308.html
http://www.space.com/scienceastronomy/mars_ice_030213.html
http://www.sciencemag.org/cgi/content/abstract/322/5899/275

Plants can beat Heat???

2008-10-16T00:17:00.003+10:00

The MSU researchers found out that the gene bZIP28 in Arabidopsis thaliana, a member of the mustard family, has ability in helping regulate heat stress.

Robert Larkin, one of the MSU researchers also stated that they have also discovered the gene bZIP28 was responding to signals from ER (endoplasmic reticulum) since it is first time that ER has been revealed as it plays a role in heat response which makes the process of tolerance of heat in plant becoming more complex.

The researches form the past has indicated that the nucleus and cytosol are two components which play a role in how plants response to heat whereas ER is responsible for proteins packaging and storing in plants.

The mechanism of how bZIP28 regulate heat is that when plant is stressed by heat, one end of bZIP28 protein anchored in ER is cut off and released into the nucleus of the cell then turn on other genes in order to regulate the response of heat.

Reference:

Article: http://www.sciencedaily.com/releases/2008/10/081006180803.htm

Image: http://www.sciencedaily.com/releases/2008/10/081006180803.htm

41397365
Chen Ting-Hao

Identical twins are not so identical

2008-10-15T23:35:00.002+10:00

The stereotype of identical twins is that they are exactly alike, share the same likes and dislikes. However despite of sharing the same genetic component, identical multiples are unique individual. Though they do share similarities, they also have many differences.

Identical twins formed when one fertilized egg splits, their DNA originated from a single source, therefore, their genetic makeup are the same and are the only people in the world with identical DNA; they are always of the same gender. On the other hand, fraternal twins are formed when two different eggs are fertilized; they are no more alike than any sibling set, sharing only about 50% of their genetic markers in a unique combination of genes from both parents. Although identical twins have the same genotype or DNA, they have different phenotypes, meaning that the same DNA is expressed in different ways.

While identical twins form with the same set of genes, human development is not just genetic. The environment also has an impact. Most of the twins grow up in the same environment; there are many circumstances that create differences in the children’s appearances, personalities, and interests. As the twins approach the teen years, they may seek to establish dissimilar qualities in order to have individual identities.

Besides environment factors, scientists also offer a new explanation for the differences between identical twins. Such differences not necessarily have to do with DNA, but in how genes express themselves. This is called epigenetic effects, which is refers to natural chemical modifications with a person’s genome. It is suggested that when identical twins are born with the same epigenome, their epigenetic profiles begin to diverge as they grow older; the differences increase as twins live longer and spend more time apart. This is because epigenetic marks are removed randomly as people aged, and environmental influences change the pattern of epigenetic marks. Gene expression and behavior is altered by a process called methylation and scientists think that a better understanding of methylation could aid cancer research.

Therefore, even identical twins having the same set of DNA, there are still differences between each of them.

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Reference:
http://www.livescience.com/health/050708_identical_twins.html

"Being male" as a disability

2008-10-15T22:34:00.001+10:00

Should men be treated as a disabled class? Men are more susceptible to emotional and developmental disorders and die in comparatively higher numbers from cancer and artery diseases than women, giving rise to the issue of legally recognizing “being male” as a disability.

The dilemma of being male starts from fetal development. Male embryos that manage to develop into fetuses have a greater risk of conditions such as perinatal brain damage and deformities. The lungs of newborn lungs of males are also more vulnerable. Males are more prone to development disorders such as deafness, blindness and reading delays and teenage boys are more likely to commit suicide or die from violent deaths before adulthood.

Men are also more medically fragile. On average, men develop coronary artery disease 10 years younger than women and experience their first heart attack 20 years younger than females. Men have weaker immune systems and are more likely to encounter serious infections. The suicidal rate of males is profoundly larger than women and 80% of the homeless are male.

These limitations may be due to having only one X chromosome or having a Y chromosome. It has also been proposed that these may be the effects of testosterone which promotes risk taking, antisocial behavior and impulsivity which leads to violence. Accumulating scientific evidence shows testosterone reduces lifetime fitness.

If maleness was classified as a genetic disorder, special entitlements and protections would take effect on males in criminal law. So far, “XYY defense” is the most widely known gender-based defense. Males born with an extra Y chromosome are suggested to be characterized with exaggerated aggressiveness and violence.

It is believed that Biochemistry will revolutionize the field of criminal law. Recent discussions have attempted to incorporate the facts arising from the Human Genome Project into the rule of law, in particular, the relationship between genes and socially constructed environmental influences. There is scientific agreement that some part of us is shaped by our environment other than genes. However, “it is certain that this information will have an impact on the way the criminal justice system looks at, and treats, criminals carrying a violence-causing genetic abnormality.” Many different categories of proof will be required before any argument of creating a different set of rules for “being male” can be made.

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References

Solomon, Louis M, Rebekka C. Noll, and Rebecca Guttman. “The Weaker Sex: Is Being Male a Legally Cognizable Defect,.” Gender “Medicine 5.3 Sept. 2008: 200-208.

The ‘scary gene” – How genes play a role in fear.

2008-10-15T22:11:00.002+10:00

Whether you are as brave as a lion (i.e. Andrew Ong), or as timid as a mouse, it seems that genes play a major role in determining how we react with appropriate fear to certain dangerous situations. Scientists have recently discovered several genes that are responsible for both innate and learned fear. Stathmin, located in the amygdala of the brain, is one of the genes that were discovered. Varying levels of this gene in humans man explain why some people are able to bungee jump or sky dive from great distances in the air without batting an eyelid, whereas others are terrified just by looking down from a few metres off the ground – although lack of common sense may play a greater role than genetics in both cases…

This discovery comes from a study conducted by a group led by Gleb Shumyatsky of Rutgers University and involved two different sets of mice - both normal and stathmin-deficient. These mice were exposed to various stressful situations, i.e. electric shock and exposure to wide open spaces, and it was found that the two different groups behaved in a very different manner. In particular, mice that were lacking in stathmin simply didn't react to situations that should have scared the rodent pants off them. [1] This was based on observations that these “daredevil” mice were reacting less strongly to electric shocks and were venturing out into environments that the normal mice would avoid (open spaces). These findings all point to the idea that amygdala-enriched stathmin is required for the expression of innate fear and the formation of memory for learned fear. [2]

So how do these findings impact the world of science and more importantly, why should we care? Well is turns out besides revealing to us that rodents not only have pants, but that they can have them “scared off” as well, this experiment serves as a template for which further research into anxiety disorders in humans can be undertaken. It also paves the way for the possible development of drugs that could either limit or enhance the effects of stathmin in humans allowing us to fine-tune our reactions to fear. [1] Who knows? Perhaps in the near future controlling pre-exam nerves may be as simple as taking one of these yet-to-be-designed drugs.

Cell Press (2005). Gene Controls Whether Fear Is A Factor. ScienceDaily. Retrieved from http://www.sciencedaily.com/releases/2005/11/051117182223.htm
Britt, R. R. (2005). Fear Factor Gene Discovered. Live Science. Retrieved from http://www.livescience.com/health/051117_fear_factor.html

By JX

Sweeter Strawberry

2008-10-15T21:03:00.002+10:00

Modification of sugar composition in strawberry fruit by antisense suppression of an ADP-glucose pyrophosphorylase

Jung-Il Park, Young-Koung Lee, Won-Il Chung, In-Ha Lee, Jae-Hyun Choi,
Woo-Moon Lee, Hiroshi Ezura, Sam-Pin Lee and In-Jung Kim

Genetics have been widely applied in agriculture. An application of transgenic technology on strawberry is to increase sugar composition in strawberry fruits carried out by group of scientists from Korea. The scientists have successfully made strawberry fruit to become sweeter in their trials.
Authors generated transgenic strawberry cultivar Anther expressing the FagpS (ADP-glucose pyrophosphorylase (AGPase) small subunit) cDNA in antisense orientation under the control of a fruit dominant APX promoter. ADP glucose pyrophosphorylase (AGPase) catalyzes the key step of starch biosynthesis. Theoretically, if the FagpS cDNA in antisense orientation works, fruit could become sweeter.
Trials were set up in glass house. Fruits at 4 different stages were analyzed to determine sugar and starch content, hardness and weight. Normally, starch content in strawberry fruit has considerable amount at green stages and decreases dramatically during the white and turning stages. In transgenic lines, the starch content was significantly lower at green stages. The transgenic fruits accumulated more soluble sugars in the red maturation phase than the control fruits. The starch synthesis was strongly repressed in the transgenic fruits by the action of anti-FagpS expression, which resulted in the increased soluble sugar content. HPLC analysis showed total soluble sugar increment from 16 to 37% in transgenic plants. Considering both sugar and starch contents in fruits, there are opposite relationship between sugar and starch accumulation. Reduction in starch synthesis in transgenic lines was transferred to the increased sucrose synthesis. Meanwhile, interestingly, most transgenic fruits did not show significant differences in weight and hardness compared to control fruit.
They concluded that fruit-specific down-regulation of the AGPase gene might be an effective strategy for increasing sugar and decreasing starch content in strawberry. This experiment is only in a small scale, but it showed that transgenic strawberry has potential to commercialize. However, before that, bio-safety including health and environmental risk assessment should be considered as, there have been a lot of debates on GMOs (genetic modified organism).
Park J., Lee Y.K., Chung W., Lee I., Choi J., Lee W., Ezura H., Lee S. and Kim I., 2006, Modification of sugar composition in strawberry fruit by antisense suppression of an ADP-glucose pyrophosphorylase, Molecular Breeding 17, Springer
http://www.springerlink.com/content/e9106284u77x730g/

DNA Markers and The Australian Beef Industry

2008-10-15T20:20:00.000+10:00

DNA Markers and the Australian Beef Industry
DNA markers and advancements of DNA technology is beginning to play an increasing role in the genetic selection of breeding animals. The advancements are making it possible to determine how production animals can be managed and bred to target specific market requirements. The majority of production traits in cattle are influenced by multiple genes; however there is a small minority of genes that control a major influence on the variation of production characteristics. These loci or QTL genes, more commonly known as “major” genes can be difficult to uncover but areas on the genetic material (chromosomes), which may be used as landmarks that are linked to these major genes, can be identified. These “landmarks” is what are understood as gene markers, in which help scientists establish as to whether an animal carries a certain major gene.
The system calculates a range gene marker values to produce a score for a particular phenotypic trait that a farmer may be targeting, with over 100 genotypic markers already understood and valued. This is translated into a score known as an EBV or Estimated Breeding Value. The EBV enables a producer to further understand the genetic make-up and breeding characteristics in which the animal may present to help target specific market requirements.
Further advancements in genetic genome technologies is increasing the accuracy of the technology, however a recent breakthrough has enabled multi-traits to be valued hence increasing the accuracy of the breeding scores as well as through the “Smart Gene” project, a genetic marker has been identified to deliver a breeding value for tenderness and marbling score of the individual animal.

A New Genetic Link to Baldness

2008-10-15T19:36:00.003+10:00

Mother’s around the world will be breathing a sigh of relief at the news their son’s baldness may not be their entire fault after all! Scientists have known for sometime that there is a genetic variant passed from mothers to sons via the X chromosome that causes men to start losing their hair around middle-age. However scientists have also long believed that several genes must be causing male pattern baldness and the quest has been on to find them.

Researchers in Canada, the United Kingdom, Iceland, Switzerland and the Netherlands have all independently found a region of DNA that appears to increase some men’s susceptibility to male pattern baldness. The newly identified region is on chromosome 20. The study analyzed the genomes of 1,125 Caucasian men who had been assessed for male pattern baldness. It then confirmed the finding on chromosome 20 in another 1,650 men. The researchers found that men, who had both genetic variations on the X chromosome and chromosome 20, have a sevenfold higher risk of seeing their hairline recede over time. As this is a new area of DNA implicated in male pattern baldness, much more research is required to establish the mechanisms involved which led to baldness and the possible treatments. Would you believe that worldwide, about $2 billion is spent each year to hide baldness! People under go transplants, they use pharmaceutical lotions, thickening agents and wigs all in an attempt to hide baldness. There is therefore a huge market to tap into but companies will have to wait as an effective treatment is many years away.

The researchers are now focusing on this region of chromosome 20. Does this area play a similar role in women? Does this area play a similar role in men from different racial backgrounds? Can a genetic test be developed to identify those most at risk of going bald? Identification of this region of DNA on chromosome 20 is a big step towards understanding the genetics behind baldness. And not to be forgotten, mothers can relax a little in the knowledge they are not totally to blame for their sons baldness!!

41779701
References:
Article: http://www.winnipegsun.com/News/Canada/2008/10/12/7063446.html
Picture:

http://www.nowpublic.com/health/end-premature-baldness-0

2008-10-15T19:04:00.005+10:00

A Million to One

In July this year, a couple of mixed parentage, gave birth to twins sons with very, very different phenotypes. That is, the twin sons were born with different coloured skin to each other. The odds against a mixed race couple having twins, who are dramatically different in colour, one black, and one white, are a million to one. The chances of this happening is certainly bewildering and unlikely, but it is no miracle.

This occurs when the woman releases two eggs; one egg encoding predominantly dark pigmentation genes and the other, fair pigmentation genes, and the 2 sperms, one with dark and fair pigmentation genes fuses together. The results of this are twins born with dramatically different coloured skin.

Skin colour is composed of up to seven different genes working together. The first generation carry half of the gene of each race, as the previous generation of parents contribute 50% of their genes to the first generation. The offsprings of the first generation, i.e. the second generation can generate various combinations. As a result, mixed race couples will produce twins with vastly different phenotypes as the alleles can come together to generate alternative combinations.

Studies have shown that if a woman is of mixed race, her eggs contain a mixture of genes encoding for both black and white skin. Likewise, a man of mixed race will have a mixture of different genes in his sperm. When these eggs and sperm unite, they create a baby of mixed race. Rarely does an egg or sperm contain genes that encode for one skin colour, either black or white, not a combination of both. The chances of this occurring are approximately 100 to one.

Some examples of couples producing twin babies with different coloured skin are: Kerry who is Nigerian and English descent, and partner is white, gave born to white twins. As the twins got older, one twin retained the light skinned colour while the other got darker. Another example is of a woman who is of Jamaican and English descent and the father is German. One twin is blue eyed blond girl, while the other is brown hair, eyes and dark skin.

41400555

Mikaylay Nguyen

http://www.dailymail.co.uk/news/article-377839/Black-white-twins.html

http://www.geneticsandhealth.com/2006/10/21/twins-with-different-skin-color-genes/

Are you at risk for nicotine dependenc?

2008-10-15T18:35:00.006+10:00

A hatred to bitter substances or an overall intensified sense of taste could help protect some people from becoming addicted to nicotine. A new study conducted by University of Virginia Health System researchers has found that two interacting genes related to bitter taste sensitivity, TAS2R16 and TAS2R38, play an important role in a person's development of nicotine dependence and smoking behavior. Researchers also found that people with higher taste sensitivity aren't as likely to become dependant on nicotine as people with decreased taste sensitivity. This new knowledge will be able to predict whether a person is apt to become a smoker or not.

It is well known that a person's ability to taste bitter substances is essential for the rejection of potentially toxic foods, but taste sensitivity varies widely among individuals and between ethnic groups. Previous studies have suggested a link between so-called taster status and nicotine dependence without taking into account the genetic evidence Until now, the method for analyzing gene to gene or gene to environment interactions could only deal with one type of trait without correcting for other important covariants, such as age or gender, but the researchers have developed an innovative, pioneering new method and corresponding computer program that can handle all types of genetic data and correct for any number of variants - gender, age, race, and so on. This new approach significantly expands our ability to study gene-gene or gene-environmental interactions, providing a far better analytical tool for every scientist out there doing genetics work.

They are paving the way for addressing nicotine dependence. On the basis of this amazing discovery, they are trying to establish a comprehensive understanding of how all associated genes work together to influence smoking behaviors and addiction and furthermore to develop effective prevention and treatment for nicotine dependence gene-environmental interactions.

Reference

University of Virginia Health System (2008, October 15). Critical Genetic Link Found Between Human Taste Differences And Nicotine Dependence. ScienceDaily. Retrieved October 15, 2008, from http://www.sciencedaily.com /releases/2008/10/081014111301.htm

41731437

Justin Won

Evolution of Beer

2008-10-15T17:39:00.003+10:00

Have you ever wondered what makes certain beers taste better than others? It turns out that genetics is responsible. Before you get visions of the ‘fittest’ of our ancestors coming up with ingenious new recipes, think again; the answer lies in a crucial ingredient to any brew and is a simple eukaryotic organism – yeast. A rare reproductive technique of this microorganism allowed the pioneer ‘geneticists’ amongst our forefathers to unwittingly produce the lager we know today.

The creation of lager began in 16th century Bavaria. Society became disappointed with the quality of ale brewed in the summer months, thus a ban was placed on brewing when it was hot. In response, brewers began to brew ale when it was cold. The low temperatures experienced in Bavaria made it impossible for the normal yeast used, Saccharomyces cerevisiae, to ferment the ale. As a result, the normal yeast hybridised with another strain of yeast, Saccharomyces bayanus, that could ferment at lower temperatures. Normally yeast reproduce asexually or, occasionally, sexually. However in this case they hybridised, which forms offspring that are essentially a new species. The resulting progeny, Saccharomyces pastorianus, contained DNA from S. cerevisiae which added the flavour, and DNA from S. bayanus that allowed the fermenting to take place at lower temperatures. The new strain of yeast that was created was able to ferment a new form of beer; what we now know as lager.

After examining DNA sequences of 17 different types of yeast used to ferment beer, researchers reached the conclusion that the hybridisation happened at least twice, rather than once as previously thought. This resulted in two broad groups of beer, called Saaz and Frohberg. In each case different amounts of DNA were found to have been contributed by each parent. One was approximately 50% of each parent, whereas the other had DNA in a ratio of 3 S. cerevisiae:1 S. cerevisiae. From these two strains, natural selection took over, as brewers favoured the variations in the yeast that made beer taste better, and those strains survived to still be produced today. Unfortunately it is unlikely this knowledge will lead to genetic modification of yeasts to create flavours, as S. pastorianus is sterile. Nonetheless, the power of genetics from centuries ago is fully evident here, and is proof that genetics can affect our lives in not so obvious ways.

Coghlan, A 2008, ‘How lager yeasts came in from the cold, twice’, New Scientist, viewed 12 October 2008, <http://www.newscientist.com/article/dn14706-how-lager-yeasts-came-in-from-the-cold-twice.html

Science Daily 2008, ‘Brewing A Great Beer: DNA Study Reveals Evolution Of Beer Yeasts’, Science Daily, viewed 12 October 2008, <http://www.sciencedaily.com/releases/2008/09/080910180844.htm>

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Are the voices in your head or in your genes?

2008-10-14T22:24:00.003+10:00

Ever heard voices in your head before? If you have, you should probably skip going to the doctor and consult a geneticist instead, according to the results of recent research into the genetic basis of schizophrenia. Schizophrenia is a relatively common psychological disorder that affects the perception and expression of reality on a mental level. Symptoms include visual and auditory hallucinations, the development of paranoid delusions, disorganised speech and thinking patterns and a general loss of social function. Approximately 0.5% of the general population suffers from this disorder. While it is accepted that schizophrenia is caused by a number of influences (environmental, psychological), there is increasing evidence that genetics plays a major role in developing this disorder. A number of alleles that contribute towards the development of schizophrenia have been identified in past studies. The presence of each allele produces a cumulative effect, increasing the risk of developing the disorder. In a recent study, twelve new single nucleotide polymorphisms were identified by comparing 479 schizophrenic patients to 2937 controls. When this was crosschecked with a larger sample size, one polymorphism stood out amongst the schizophrenic patients. This gene, ZNF804A, codes for a DNA binding protein. While its function is currently unknown, it is believed to be involved in DNA transcription regulation. In a similar study, an allele of the gene CACNA1C was found to contribute to schizophrenia. This gene codes for a calcium ion channel subunit, suggesting that it is involved with cell communication. Together these studies increase our knowledge about schizophrenia and its genetic causes. It is a necessity that further studies pursue other contributing alleles in order to build up our knowledge. With enough research, it may even be possible to develop a genetic test that quantifies a person’s risk of developing schizophrenia. This would be of great benefit to mankind.

Source - http://www.phgfoundation.org/news/4369/

Stem cell hope for hearing loss

2008-10-14T16:07:00.000+10:00

Have you ever turned up your mp3 player and blasted your eardrums with the latest hit song? This may seem innocuous and part of the youth culture of today, but prolonged exposure to loud noise can severely damage the delicate hair cells in the cochlear. Responsible for hearing, the small hair cells are found in the spiral shaped cochlear and detect different frequencies of sound based on tiny differences in length. Stimulation of these cells sends action potential impluses to the brain and thus we are provided with the sensation of hearing. When damage occurs, such as that cause by loud noise, it is difficult for the body to naturally repair these cells. By the time the effects are fully realized, it’s too late. The damage is already done and results in hearing impairment or in extreme cases, deafness.

With an entire generation already constantly plugged in to their headphones, we’re heading for an epidemic of hearing loss in the future. Currently treatments for this kind of damage are extremely limited, focusing more on increasing the sound channeled directly into the deafened ear (i.e. certain modern hearing aids). Prevention is obviously best, but what if prevention is too late? In those cases, what if the damaged hair cells could be replaced to restore hearing? Dr. Robert Miller and Dr. Kumar Alagramam of Case Western Reserve University School of Medicine recently published research into new methods of treating hearing loss. “Cochlear stem cells” have been found which readily develop into ear related tissue. For further proof, postnatal mouse cochlea tissue was cultured into “stem cell” spheres, then using a hair cell development marker, it was confirmed that hair cell precursors could be produced from stem cells existing in cochlear tissue.

In early life the stem cells have the ability to regenerate hair cells and from this new hearing loss treatments could be developed, like transplanting cochlear stem cells into an adult cochlea or researching compounds that could activate this transition. Extensive research has to be conducted before hearing restoration treatments become part of a hospital’s repertoire, but hopefully this research will produce treatment options available to the future sufferers of hearing loss.

References:
Case Western Reserve University (2007, April 6). Isolation Of Stem Cells May Lead To A Treatment For Hearing Loss. ScienceDaily. Retrieved October 14, 2008, from http://www.sciencedaily.com /releases/2007/04/070405170200.htm

By Madelyn Loadsman
(41747849)

Potential Cure for Rare Genetic Disease

2008-10-14T15:49:00.010+10:00

Tuberous sclerosis is a genetic disease that causes benign tumors to grow on various vital organs of the body such as the skin, liver, kidney, lungs and brain. Although non-cancerous, these growths cause seizures, epileptic attacks, skin deformities and lung and kidney disease. Additionally, up to 50% of tuberous sclerosis victims suffer from learning difficulties, ADHD and out bursts. Other studies have reported between 25 – 68% of victims diagnosed with autism.

A human with tuberous sclerosis is shown to have a mutation in the genes TSC1 and TSC2 which syntheses an overly active form of the protein mTOR which results in tuberous sclerosis.

Fortunately a study in the UK at Cardiff University has discovered a chemical found on Easter Island that could potentially aide in the treatment of this disease. Sirolimus, identified in a soil sample, has been claimed to affect the two disease causing genes which could possibly control the mTOR protein.

Sirolimus is currently on the pharmaceutical market as an immuno-suppressant drug used to prevent rejection during organ transplants, known as Rapamune.

The studies on tuberous sclerosis patients with kidney tumors and lung disease with the administration of this drug are not yet completed. As of early this year it was reported that the average diameters of the various tumors treated with Sirolimus decreased in size by approximately 26% and simultaneous studies in America have described similarly spectacular findings.Currently phase three clinical trials are taking place successfully in that they are reducing tumor size but unfortunately the majority grow back once the treatment is ceased. Hopefully someday Sirolimus will be suitable and available for the successful cure of tuberous sclerosis permanently.

Birds have a well-developed sense of smell

2008-10-12T22:57:00.004+10:00

It was previously thought that birds have only sight and hearing well-developed, but a study carried out by Silke Steiger and her colleagues at the Max Planck Institute for Ornithology extends this to smell as well.
The team did research on the olfactory receptor (OR) genes, which are expressed in sensory neurons of the olfactory epithelium. They found out that various scents that can be distinguished and perceived by an animal may depend on the total amount of OR genes present in the animal’s genome.

Researchers compared the OR genes of eight remotely related species of birds and made estimates on the total amount of OR genes in each species’ genome. They discovered that the amount of OR genes can vary. For instance, the brown Kiwi from NZ has approximately six times more OR genes than the canary.
Furthermore, the researchers found out that the number of genes is linked to the olfactory bulb’s size, and this is quite logical as the function of the olfactory bulb is to process olfactory information.

Indeed, different ecological niches could have made an impact on the amount of genes present in birds. For instance, the Kiwi bird is nocturnal and hunts for food at night. It is reasonable that they rely on their sense of smell instead of sight and hearing.

In addition, the researchers were able to make predictions on the amount of OR genes which were functional. In humans, only about 40% of all the OR genes are functional. This could well be due to mutations in the OR genes which render them non-functional. As a result, humans have a poorly developed sense of smell when compared to other mammals. In contrast, the bird species have a greater proportion of functional OR genes, which shows birds as having greater reliance on their sense of smell.

The chicken genome was sequenced three years ago and a new class of OR genes was discovered. Steiger and the other researchers have demonstrated that these OR genes are a common feature amongst birds, yet these OR genes are not present in other vertebrates. The precise function of this type of OR genes is still unknown.

Reference: Max-Planck-Gesellschaft (2008, July 16). Birds Have A Good Sense Of Smell. ScienceDaily. Retrieved October 12, 2008, from http://www.sciencedaily.com/releases/2008/07/080716111421.htm

By Priscilla Chau (41794290)

Born To Smoke?

2008-10-12T17:15:00.002+10:00

A new study conducted by Sherva et al. has identified a link between first experience with smoking and the likelihood that a person is currently smoking to a genetic variation in the CHRNA5 nicotine receptor gene. This discovery will act as a stepping stone for researchers to elucidate the reasons why for some people, the first cigarette experience might’ve been extremely unpleasant but for others, the first puffs were accompanied with a rush of euphoria and pleasure. This new finding will undoubtedly bring more attention to the growing suspicion surrounding the role of a particular nicotine-receptor gene in smoking-related behaviours and in the development of lung cancer. Based on the experiment, Sherva et al. noticed that regular smokers were more likely than never-smokers to have the less common rs 16969968 form of the CHRNA5 gene, a variation which stems from one different base-pair in the gene sequence from the more common form. This genetic variation is known as a single nucleotide polymorphism (SNP). In addition, smokers were also 8 times more likely to indicate that their first cigarette gave them a pleasurable rush. This finding bolsters the postulation which suggests that the initial physical reaction to smoking and his/her consequent behavior toward the habit is determined by the person’s genetic makeup. The association made between genetics and pleasurable early smoking experiences may justify how addiction is initiated. Nonetheless, genetic variant explains only a fraction of human smoking behavior as social influences and other environmental factors interact with genes too. Sherva et al also notes that the same single nucleotide polymorphism, rs 16969968, of the CHRNA5 gene is also associated with smokers’ level of nicotine dependence and that variations in the same gene and related genes significantly increases an individual’s risk of lung cancer. So, in light of this latest discovery, are smokers now in a position to freely blame their cigarette addiction on their genetic makeup, knowing that the risk of developing of lung cancer has also already been pre-determined and, therefore be rid of the conscience to quit this disgusting habit?
41723151
References: 1) http://www.medicalnewstoday.com/articles/117767.php
2) http://viraltrivedi.files.wordpress.com/2007/08/cigarette_butt.jpg (picture)

Chicken eggs in drug industry?

2008-10-10T13:53:00.001+10:00

Most people might have heard that chicken eggs can be used to make vaccines by injecting flu virus into a fertilized eggs, however scientist have now raised the stage and have created a genetically modified rooster that produces offspring that lay eggs than be used as medicine instead of protein. Scotland researchers, Helen Sang and her colleagues of the Roslin Institute in Edinburgh, produced variety of drugs inside a fertilised chicken embryo by inserting a certain gene with lenti-virus hence replacing the protein oval brumin. Then by breeding the chickens with the new gene found in its semen, it was possible to produce descendants that carried the wanted gene. The chickens can then lay eggs that contain medicines inside the whites of their eggs.

Recent studies showed that the medicine egg can produce miR24, a monoclonal antibody that is used to treat melanoma or interferon b 1a, and immune system protein that can be used in the treatment of multiple sclerosis. However, this is dependent on the type of gene inserted in creating the chickens.

It is now only a matter of time before the new medicine eggs to be used to make drugs for human consumption and replace other genetically modified products used in pharmaceutical industries such as goat milk.

4137654
References:http://www.sciam.com/article.cfm?id=the-incredible-medical-eg

Don't surrender any more tooth fairy

2008-10-10T13:51:00.001+10:00

After years of focusing its efforts on stem cells found in the root apical papilla, tissue connected to the tip of the root that is responsible for the root’s development, an international team headed by dentistry researcher Songtao Shi in a University of Southern California has finally determined the ability of stem cells from extracted teeth to regenerate tooth roots.

Shi and his colleagues compared the performance of apical papilla cells to pulp cells both in vitro and in mouse samples in order to determine the appropriate stem cells for creating a new root. As a result, the apical papilla cells was chosen to be the right stem cells to be used as it provided better tissue regeneration which leads to the formation of all root tissues as well as the support substances (dentin and cementum) in the crown and root. Shi’s team then replaced an incisor extracted from a miniature pig, which has a similar dental structure to humans, with stem cells from the extracted wisdom teeth of 18- to 20-year-old humans.

The experiment achieved successful outcomes. Three months after the implantation of the stem cells, the researchers successfully fitted a porcelain crown over the mineralized roots and ligaments developing there. After six months the tooth had a strength that was "not quite as strong as the original tooth, but we believe it is sufficient to withstand normal wear and tear" says Shi.

According to George T. Huang, a professor of dentistry at the University of Maryland, Shi's finding has a great potential in resolving problems of implants. Loosening and increased risk of gum disease are the two main problems of implants caused by an “unnatural relationship with the bone”. A ligament layer between the jawbone and the root itself in the original tooth, however, can solve these problems as it serves both to adhere the tooth to the jaw and to provide a cushion during biting.

Although the research is still in the early stages, it is a promising step towards discovering potential clinical applications that would have a big impact on oral surgery procedures such as root canals.

By So Young Lee (41774171)

References:

Nikhil Swaminathan, 2006, Don’t surrender any more teeth to the tooth fairy, Scientific American, viewed 9 October 2008, http://www.sciam.com/article.cfm?id=dont-surrender-any-more-t

Treating Cancer Before It Starts?

2008-10-10T13:48:00.002+10:00

Treating cancer before it starts? It is a possibility, according to the latest findings in molecular research by Dr. Alex Deiters (assistant professor of chemistry at North Carolina State University). In recent months, a molecule has been examined that can potentially stop the production of cancer cells at the very beginning of their development by altering the function of gene regulators.

In the human body, gene regulators (or gene ‘programmers’) known as microRNA’s are responsible for the conversion of healthy cells into cancer cells. Residing in every cell in the human body, these single stranded microRNA’s are made up of about 20nucleotides and are involved in more than 30% of all processes of gene regulation in the healthy body (they have the ability to shut down genes and prevent their expression). In outstanding circumstances, such as in cancer patients, these miRNA’s have been misregulated, resulting in either over or under expression of particular genes.

According to findings by Deiters’, these genetic regulators would be an excellent target for cancer drug therapies, and they are a “largely unexplored class of targets for the development of therapeutics and diagnostics”. Because miRNA’s have the ability to prevent gene expression, they have the potential to be more effective in therapy due to higher selectivity than chemotherapy drugs. As well, adverse effects are predicted to be more minimal.
Research at NC State Univeristy has involved one miRNA in particular- miRNA-21. It is responsible for rapid cancer cell growth, and has been linked to cancers such as glioblastoma, which is currently thought to be responsible for 52% of all brain tumours and is extremely difficult to treat. Researchers hoped that preventing production of miRNA-21 by 80% would lead to glioblastoma cell death. Results showed that decreasing the level of miRNa-21 lead to an increased susceptibility of the cancer drugs to traditional therapy, although they were not able to prove that glioblastoma cells were destroyed outright.

After testing more than 1200 seperate compounds, researchers have discovered the first small molecule that inhibits miRNA-21 production. Although there is a long way to go in research, this discovery has given rise to the possibility of the development of new drugs that can treat some of the most aggressive forms of cancer.

------------------
By Eleanor Rose, 40972783

Stopping Cancer cells Before they Start? Inhibitor of Gene Regulator Discovered.
http://www.sciencedaily.com/releases/2008/09/080924184657.htm

Feeling a little bit retro?

2008-10-10T01:42:00.008+10:00

Its little doubt that virus’s are in everyday life; we see their effects everywhere. Influenza, skin infections, chicken pox are all examples about how virus’s can make life miserable. These so called “discarded evolutionary shells” however are only recently becoming understood. The public still view them as cyto-terrorists fully equipped with a scant arsenal with which to hijack a cell’s biochemistry, and they are quite justified. In actual fact, the variation of biochemistry within the viral world far outstrips that of the realm of the cells. Many have pondered the complexity of the virus, with its novel ways to package and produce genetic material, but it is just really the tip of the iceberg. New evidence has emerged that suggests in no uncertain terms that viruses not only shape our lives today, but have had a key role in shaping our very beginnings as living organisms.

According to some of the top virologists, the virosphere has only truly been explored in the last few years, with some astonishing results that provoke further thought into the oft shafted DNA cast offs. Patrick Forterre, a virologist from France has put forward the notion that virus DNA has played key roles in the evolution of all living species “Geneticists have discovered that the genomes of every living organism appear to be laden with the remains of ancient viral infections. In eukaryotes, the most complex domain of cellular life including humans, the main source of this DNA is retroviruses - RNA viruses that, after infecting a cell, convert their genome into DNA and integrate it into the host. Sometimes they become a permanent addition, called an endogenous retrovirus, or ERV.”

Patrick goes on to further demonstrate that past viral infections have left major twists on evolution. He and fellow virologists stipulate that at least 8% of human genes are a product of past retrovirus’s, with another 40-50% looking highly suspicious. This “raining of viral DNA into genomes” is not confined to humans: rodents, apes, monkeys and koalas have also shown enormous amounts of viral leftovers. Everywhere geneticists look they are finding more and more ERV’s that seem to be beneficial viral cast offs.

It seems that there is more than a little bit of virus in all of us.

s4172657 H. Singh

Source: Garry Hamilton. Viruses: The unsung heroes of evolution.
New Scientist August 27 2008.

http://www.newscientist.com.ezproxy.library.uq.edu.au/channel/life/mg19926711.600-viruses-the-unsung-heroes-of-evolution.html

Transgenic tomatoes = Alzheimer’s vaccine

2008-10-09T22:09:00.003+10:00

Alzheimer’s disease is a neurodegenerative disease and is the most common cause of dementia. It is thought to be caused by the accumulation of beta-amyloid, a toxic protein in the brain, resulting in neuronal death. Reducing the accumulation of beta-amyloid may inhibit the degeneration of the nervous system, delaying or potentially preventing Alzheimer’s disease. Recent studies focus on developing a vaccine using the beta-amyloid peptide. Due to the toxicity of the protein, numerous problems are associated with the production of beta-amyloid in micro-organisms. As such, scientists are investigating the possibility of the protein production in plant cells. Previous studies have shown that antigens produced in plant cells can induce immune responses when orally delivered to animals. Tomatoes are ideal candidates as vaccine carriers because they can be eaten without heat treatment, which may potentially destroy the immunogenicity of the antigen.

Kim’s aim was to develop a plant-derived vaccine against Alzheimer’s disease. Kim and his colleagues analysed the ability of tomato-derived beta-amyloid antigen to evoke antibody responses in mice. The researchers inserted the beta-amyloid gene into the tomato genome. To measure the immune responses to the tomato-derived toxic protein, they immunized the mice orally with the transgenic plants once a week for three weeks. In addition, the scientists gave the mice a booster seven weeks after the first feed.

Blood analyses showed a strong immune response after the booster with a production of serum antibodies against the beta-amyloid antigen. The results concluded that the beta-amyloid protein can be produced in transgenic tomatoes and used as a delivery system for the oral immunization of mice. However, as such low levels of the protein were expressed in the transgenic tomato plants, the team is currently investigating strategies to increase the potency of the tomato-based vaccine. Although a reduction in beta-amyloid was not observed, based on previous studies similar results can be expected in that induced serum antibodies will result in the reduction of beta-amyloid.

Although the research is still in the early stages, it is a promising step towards discovering an edible vaccine against Alzheimer’s and paves the way for more potential vaccines.

Charmaine Lee
41778236

For more information:
Youm J, Jeon J, Kim H. Transgenic tomatoes expressing human beta-amyloid for use as a vaccine against alzheimer’s disease. Biotechnol Lett 2008 May 30 1839:45
http://www.springerlink.com/content/63756gk168471265/fulltext.pdf

Mothers Turn Fearless When Peptide Level Drops

2008-10-09T11:27:00.004+10:00

Everyone knows not to get between a mother and her offspring. What make these females unafraid when it comes to protecting their young may be low levels of a peptide, or small piece of protein, released in the brain that normally activates fear and anxiety, according to new research published in the August issue of Behavioral Neuroscience.

"We see this fierce protection of offspring is so many animals," says Stephen Gammie, a University of Wisconsin-Madison assistant professor of zoology and lead author of the recent paper. "There are stories of cats rescuing their kittens from burning buildings and birds swooping down at people when their chicks are on the ground."

In terms of biology, it makes sense that mothers would lay down their own lives to protect their offspring, especially if it means the parents' genes will be passed down to the next generation, says Gammie. But he adds that despite all the observations and the theories explaining why mothers display this behavior - commonly known as maternal aggression - very little research has investigated the biological mechanisms that turn on this trait in new mothers.

"We've known for a long time that fear and anxiety decrease with lactation," explains Gammie. "Maybe it's this decrease that allows mothers to attack during a situation that normally would evoke a fear response."

Testing this hypothesis, the Wisconsin professor and his colleagues studied the link between maternal aggression in mice and levels of corticotropin-releasing hormone (CRH), a peptide that acts on the brain to control behavior.

About six days after a group of mice gave birth, the new mothers received injections containing either one of three doses of CRH or a saline solution with no amount of the peptide. Following each injection, which was given once a day for four consecutive days, the researchers returned the mother mice to their pups. Twenty-eight minutes later, the researchers removed the pups and introduced a male intruder.

Under normal conditions, female rodents will fiercely attack the males, says Gammie, noting that the males sometimes eat pups and that "the best defense for the mom is the offense."

For the study, only the mice that received either no dose or a low dose of the peptide displayed the expected behavior. As the levels of CRH increased, the number of attacks and the duration of them dramatically decreased.

The results show, for example, that while the mice with the lowest levels of CRH attacked more than 20 times for the duration of about 45 seconds, the mice with moderate levels of the peptide attacked about six times over about eight seconds. Mice with the highest levels of CRH didn't attack at all.

"When we put the male in the cage, some moms would just sit there. They weren't protective at all. If anything they were skittish. They showed a fear response," says Gammie.

The researchers note that altering the levels of the peptide appeared to affect only maternal aggression; normal maternal behaviors, such as nursing, were observed in all mothers both before and after the encounters with male mice.

Based on the results, Gammie says, "Low CRH levels appear to be a necessary part of maternal aggression. If you don't keep them low, you won't see this fiercely protective behavior."

He adds that this finding - some of the first evidence suggesting a biological mechanism that enables parents, regardless of the potential danger, to defend their offspring - may also begin to explain why mothers occasionally neglect or harm their offspring.

"Postpartum depression in some individuals has been linked to higher levels of CRH release and an overly active stress response," explains Gammie. "If CRH needs to be low to see maternal protection of offspring, as our work suggests, then it explains why moms with high postpartum depression and high CRH not only may neglect, but also may abuse, their children."

Reference: Science Daily website - http://www.sciencedaily.com/releases/2004/08/040801231328.htm

Cheung Lok Hang 41376810

“Engine” which drives cell movement discovered

2008-10-09T10:02:00.010+10:00

For the first time researchers have managed to determine how a cell assembles its internal mechanisms in order to carry out cell movement.

This groundbreaking research carried out by Thomas Leung, Ph.D., and his team in the GSK-IMCB Group at the Institute of Molecular and Cell Biology in Singapore, is essential to the understanding of how a cell responds to its external environment.

The researchers discovered a complex of three proteins (known as MRCK, LRAP35a and MYO18A) that directly controls the myosin network within a cell, as a result generating traction force to propel the cell forward. (Myosin is a protein found in muscle cells, which is responsible for the elastic and contractile properties of muscle. A different form of myosin is involved in cell movement.)

This action of the tripartite protein complex may be compared to a spring in a toy car – when the protein complex assembles and moves backwards within the cell, it resembles the wound up "engine" of the toy car that has been pulled backwards. Thereafter the disassembling of the protein complex results in a forward movement of the cell which can be likened to the released spring which releases the potential energy which was previously stored to drive the car forward.This discovery is predicted to have extensive implications in the fields of cancer growth and spread, wound- healing, learning and memory, and developmental biology.

By 41783810

Reference:

Agency for Science, Technology and Research (A*STAR), Singapore (2008, October 7). Landmark Discovery Of 'Engine' That Drives Cell Movement. ScienceDaily. Retrieved October 9, 2008, from http://www.sciencedaily.com /releases/2008/10/081006102609.htm

Is Homosexuality In Males Genetic?

2008-10-09T10:00:00.003+10:00

Several lines of evidence have implicated genetic factors in homosexuality, the most compelling observation has been the reportof genetic linkage of male homosexuality to microsatellite markerson the X chromosome. A study was conducted in Canada including 52 gay male sibling pairs, and their close family.

In past experiments, there was supposedly evidence of the 'homosexuality trait' being involved with the X-linked geneat position Xq28. This was based on family recurrence patterns and molecularanalysis of the X chromosome in families in which there were multiplebrothers with homosexual orientation. However, the evidence for X linkage has been questioned on theoretical and empirical grounds

Nevertheless, it has been shown in many cases that there is a link with sexual orientation and twins. Twin studies have shown increased concordance for homosexual orientation in monozygoticas compared to dizygotic twins. On the other hand,the similar rates of male homosexuality in biological and adoptivesiblings of male homosexual index subjects, coupledwith methodological uncertainties in family and twin studies ofhomosexuality, suggest caution in accepting a genetic-epidemiologicalbasis for homosexuality.

The nature of these experiments have yet to have the scientific weighting behind the allegations, however when certain data is shown, a definite linkage can be seen.

Reference: http://www.sciencemag.org/cgi/content/full/284/5414/665
41761676 Jack Morgans

Cheap Genome Sequencing Announced!

2008-10-09T09:36:00.004+10:00

We've all heard that in order to have our entire genomes sequenced it would cost us maybe hundreds of thousands of dollars or even millions of dollars some decades ago. You might have heard that it can be done with only a few thousand dollars in the near future. Well, now you can have it done for only 5000 dollars.

Complete Genomics Inc. has finally announced its formal launch for large scale human genome sequencing. Complete Genomics is a company in San Francisco and have been operating silently for two and a half years reinventing the process of genome sequencing towards completion and now it has been.

One of the aims of complete genomics is to provide high-quality, high-throughput, affordable, complete human genome sequencing services for medical and pharmaceutical benefits. This new technology's high accuracy and low cost approach will be targeted towards pharmaceutical and biotechnology companies as well as medical researches that were previously priced out of the market.

Reference:
http://www.medicalnewstoday.com/articles/124572.php

41618024
Michael Ngo Tien Yung

Gene discovery may help hunt for blindness cure

2008-10-09T06:42:00.006+10:00

Scientists have discovered a gene mutation linked to the most common cause of blindness in the developed world, holding out the prospect of better treatments and perhaps eventually a cure.

British scientists said on Tuesday they had found six variants within the gene called Serping1 that were associated with age-related macular degeneration (AMD).

AMD -- which involves damage to the delicate cells of the macula, a region at the center of the retina -- is increasingly common as people get older.

*Macula
A small, highly sensitive part of the retina of the eye of many vertebrates, which is responsible for detailed vision. In certain vertebrates, including primates, a region called the fovea – the site of greatest visual acuity – lies at the center of the macula.

Around 90 percent of patients diagnosed with AMD have the so-called dry version,
for which no treatment is currently available.

The rest have wet AMD, which occurs when tiny new blood vessels grow between the retina
and the back of the eye.
This form of the disease can be treated with modern drugs.

http://www.newsdaily.com/stories/tre49620s-us-blindness-gene/

www.daviddarling.info/encyclopedia/R/retina.html

4113667 Kyu Hyung Lee (Roy)

Green Fluorescent Protein: Lighting The Way To A Cure

2008-10-09T01:17:00.002+10:00

The Nobel Prize is the pinnacle of success for scientists worldwide. But what sort of research could possibly result in the presentation of such a prestigious award? The three award recipients of the 2008 Chemistry Nobel Prize received the award for their research into a biofluorescent protein found in the jellyfish Aequorea victoria. This protein lights up green when placed under blue light. Scientists have long known of the presence of green fluorescent protein (GFP) within jellyfish and other marine life; however it has only been applied to a variety of uses in recent times.

The major application of GFP is for use as a marker within cells. The advantage of using GFP rather than other fluorescent markers within cells is that GFP is not toxic to cells. This is because it is a natural protein which is expressed by the cell, whereas other fluorescent markers are used to stain cells. This brings about the possibility of observing cells which are unseen without GFP over a period of time.

Researchers at the Cedars-Sinai Medical Center’s Maxine Dunitz Neurosurgical Institute, along with others from Lund University, have exploited a virus to carry GFP. This virus was injected into the brain of rats that suffered Parkinson’s disease. The purpose of the research was to investigate the effect that two genes responsible for the genesis of new neurons (neurogenin2 and noggin) had on the areas of the brain affected by Parkinson’s. The study showed that neither gene was capable of stimulating the production of new neurons; however noggin contributed to an increase in the number of ogliodendrocytes present in the affected area. While this study was not a success, it has provided a starting point for research into treating Parkinson’s, while paving the way for research into a number of other diseases.

41755040

References:
http://www.sciencedaily.com/releases/2008/09/080903172407.htm
http://www.newscientist.com/article/dn14895-chemistry-nobel-for-green-jellyfish-protein.html?DCMP=ILC-hmts&nsref=specrt11_head_Protein%20prize

The Tables Have Turned: GM Foods Wipe Out Global Famine

2008-10-08T22:09:00.004+10:00

Agricultural biotechnology has the potential for huge impacts on many facets of agriculture- crop and animal productivity as well as yields stability, environmental sustainability and consumer traits. There has always been an ongoing debate about genetically modified (GM) foods across the world. In Europe, there has been an introduction of regulations regarding the distribution of genetically modified foods, which ultimately limits their widespread use by consumers.

Recently, myths surrounding “Frankenstein foods” have been dispelled by the effective use of genetically modified foods in agriculture. A recent development in GM cotton farming introduced transgenic cotton. This discovery allowed for great improvements in health and financial income levels of eleven million cotton farmers. There will soon be benefits in the food field where there aren’t so many at the moment. A prime example is the papaya crop in Hawaii, which was saved by genetically modified papaya. The modified fruit aptly dealt with the detrimental effects of pest invasion. GM foods have the capability to eliminate disease and are also as a more efficient form of agriculture. GM food enables farmers to grow more crops from the same amount of acreage in a world where there are starving populations. It also enables farmers to grow the crops with less use of insecticides, or fungicides or weed killers.

There has been a great deal of propaganda that has made society produce an ideological opposition against GM foods. Already, Americans have been exposed to GM for over ten years and no legal case has been made against any product. The sudden boom of world food prices and the scarcity of natural resources of food have encouraged agricultural biotechnology developments. The threat of future world famine is looming, where there were once grain mountains there are now shortages. People are beginning to recognise that the world is in desperate need of the most efficient form of agriculture that is GM foods. For this technology to develop further, the politicians must work in conjunction with scientists and food retailers in order to promote the proper use of GM and help fight the outbreak of global famine.

Stavroula Prokopiou
41793565

References:
Cooke, Jeremy ‘GM Food: Monster or Saviour?’ BBC UK News 2008, viewed 28 September 2008, http://news.bbc.co.uk/2/hi/7426054.stm

Firpo-Cappiello, Robert ‘Building better Veggies’ Men’s Journal 2006 viewed 28 September 2008 http://mensjournal.com/healthFitness/0612/nutrition_veggies.html

Gene Mutation, Leading Factor to Skin Cancer

2008-10-08T18:37:00.005+10:00

It is generally known that people with pale skin and light hair will more likely to develop skin cancer due to lesser pigmentation to protect skin from ultraviolet rays. This increases the chance of developing melanoma.

However researches showed that besides pigmentation, gene mutations can be one of the leading factors to skin cancer. There are two main types of genes that are identified in this case.

First of all, the two mutations in gene ASIP doubled the chances of developing melanoma. This gene, which is closely related to the production of red hair and freckles, is therefore affecting the risk of getting skin cancer. This is being tested on people from Iceland, Sweden and Eastern Europe.

Secondly, mutations of gene MCIR would increase the possibility of getting skin cancer. Gene MCIR affects a person’s skin tone by causing a person to have red hair and freckles. Therefore this gene will affect the chance of a person in getting skin cancer.

On top of all these, sun exposure plays an important role in causing skin cancer. This can be proved by observation of these gene mutations has little effect on people in Arctic. This is mainly due to the lack of exposure to sun in Arctic.

In conclusion, besides pigmentation, the gene that regulates skin tone plays an important role in affecting risks of getting skin cancer. Thus by understanding the structure of gene and controlling skin tone of a person, we can save lives by eliminating the risks of melanoma development.

References:

Calloway, E 2008, Skin-tone gene could predict skin cancer, NewScientist.com, viewed 03 October 2008, http://www.newscientist.com/channel/life/genetics/dn13922-skintone-gene-could-predict-cancer-risk.html.

Behind Blue Eyes

2008-10-08T12:23:00.006+10:00

In the human population, blue eyes, a recessive trait, is quite a rare characteristic. Instead, it is more common to find individuals with brown eyes. Recent research has found that people with blue eyes share a common ancestor. Scientists believe that between 6000-10000 years ago, genetic mutation that resulted in blue eyes characteristic occurred to one person. As it is more likely for Europeans to have blue eyes, this individual was believed to have probably originated from the northwest part of the Black Sea region. This region was where the great agricultural migration of the northern part of Europe occurred during the Neolithic period.
According to Professor Hans Eiberg from the Department of Cellular and Molecular Medicine at the University of Copenhagen, all humans originally had brown eyes. The gene responsible to give eyes their brown colour is OCA2 gene. This gene encodes for P protein, which involves in the production of melanin, a pigment which can also be found in dark skin. In the case of people with blue eyes, mutation of OCA2 gene occurred, turning off the “switch” and slowing down the production of melanin. This occurrence diluted the brown colour and hence causing the iris to become blue.
Blue-eyed individuals have small degree of variation in the area of their DNA that is responsible in controlling melanin production. Therefore, Professor Eiberg and his team concluded that individuals with blue eyes are related to one ancestor as they all have the same switch on the same spot in their DNA. The mutation of brown to blue eyes that occur thousands of years ago had contributed to genetic diversity of human today.

References:
1. http://www.thespec.com/News/CanadaWorld/article/317579

2. http://www.dailymail.co.uk/sciencetech/article-511473/All-blue-eyed-people-traced-ancestor-lived-10-000-years-ago-near-Black-Sea.html

3. http://www.physorg.com/news120933651.html

41479391

The Genetics of congenital hearing impairment

2008-10-08T10:43:00.001+10:00

Advances in human genetics have facilitated procedures regarding diagnosis and treatment of various pathological conditions. Hearing impairment is an extremely prevalent sensory disorder with a genetic etiology in more than 50% of cases. Mutations in approximately 44 specific genes have been found to be responsible for these cases. Providing a genetic diagnosis in congenital hearing impairment has implications for many aspects of the management of this condition. The prognosis, the possible risk of associated medical manifestations and the precise genetic counselling of the family, are all affected heavily by an early genetic diagnosis. It is therefore important that this is integrated into the medical examinations performed.
Large-scale mutation detection methods are promising for wider genetic testing, but due to significant ethical issues associated with clinical studies, very little research has been performed. The clinical evidence currently available is insufficient to justify genetic screening for mutations specifically associated with hearing impairment. Without the necessary research hearing impairment, and many other conditions with genetic etiologies, will continue to cause mortality and morbidity within our society.

Reference:
Tranebaerg, L. 2008, ‘Genetics of congenital hearing impairment: a clinical approach’, Int J Audiol, vol. 47, no. 9, pp. 535-545.

Circulating mutant DNA to assess tumour dynamics.

2008-10-08T10:02:00.002+10:00

Recent developments in cancer diagnosis are the testing for mutant DNA fragments in the blood. DNA containing somatic mutations is highly tumour specific and thus, in theory, can provide optimum markers. They found that by monitoring the presence of these mutant gene fragments they could monitor tumour dynamics in patients undergoing chemotherapy or other cancer treatments.

Unfortunately the numbers of mutant DNA fragments circulating in the blood stream are usually small in comparison to the numbers of normal circulating DNA fragments. This can make it extremely difficult to detect and quantify them. In this study a highly sensitive approach to detecting and quantifying was used and they were successfully able to monitor tumour dynamics in a number of patients undergoing surgery or chemotherapy.

These advances greatly benefit society by making the diagnosis of cancer both more accurate and less invasive.

Article available at:
http://www.nature.com/nm/journal/v14/n9/full/nm.1789.html

A Second Chance for the Extinct

2008-10-07T20:22:00.004+10:00

Once a species is extinct that’s it for that species. Right? Think again. Scientists from Yale University have found that it may be possible to revive some extinct species of Galapagos tortoise.
It’s a commonly known fact that dog species can interbreed, but were you aware that tortoises can? Using genetic markers from over 2000 tortoises from the Galapagos islands, scientists have created a genetic profile of every population on the Galapagos archipelago. With this genetic profiling some very interesting aspects of the tortoises’ genes have come to light. Species and taxons of tortoise were identified, allowing scientists to recognize tortoises which contain mixed DNA. In current populations of tortoise both distinct lineages of tortoise and intermingled species of tortoise were found to be present. Most importantly it was found that tortoises on Volcano Wolf contain genetic traces of an extinct species of tortoise called the Floreana Galapagos tortoise. The DNA of tortoises on Volcano Wolf contain not only the mitochondrial DNA but also the nuclear markers of the Floreana species of tortoise.
Scientists believe this interbreeding may have occurred when fishermen, whalers and pirates would take tortoises as pets, leaving them on Volcano Wolf, being the last stop before heading across the ocean. Before picking the tortoises back up, if they came back at all, the tortoises would have had the opportunity to mate passing on the distinct DNA of their species to others of a different species. With careful breeding, scientists believe they may be able to crossbreed tortoises to contain large amounts of Floreana DNA. They believe in time they may even be able to revive the Floreana species, bringing animals back from extinction.

By Jolinda Cranitch, 41769832

Yale University (2008, October 2). Extinct May Not Be Forever For Some Species Of Galapagos Tortoises. ScienceDaily. Retrieved October 7, 2008, from http://www.sciencedaily.com /releases/2008/09/080923091341.htm

Of Contraception and Love

2008-10-07T01:40:00.004+10:00

Have you ever thought that besides the minor side effects caused by contraceptive pills such as irregular bleeding or spotting, nausea, weight gain and mood changes, contraceptive pills may also desensitize a woman's sense of smell, hence disrupting women's natural ability to choose a partner that is genetically dissimilar to themselves. Although contraception is not the major culprit for every bad relationship, new research discoveries at the University of Liverpool in the U.K. could help explain how people find their ideal love. In order to maintain genetic diversity among the human population, humans generally select their partners through body odour as it is believed that by exhibiting a different genetic profile from your partner, hence higher chances of variation, the offspring will inherit the ability to resist a wider range of diseases.

Natural odour reflects a person's immune system composition. Genes in the Major Histocompatibility Complex (MHC) which is responsible in building proteins involved in the body’s immune response, also play a major role in odour through interaction with bacteria in skin. As people tend to be attracted to others with a different genetic make-up to themselves, the genes in MHC are able to help in deciding which individuals find us attractive.

To further explore the effect of birth control, Craig Roberts, a Lecturer in Evolutionary Psychology who carried out the work in collaboration with the University of Newcastle analysed how the contraceptive pill affects odour preferences by getting one hundred women to indicate their preferences on six male body odour samples which were drawn from 97 volunteer samples, before and after initiating contraceptive pill use. Roberts found that women who began using contraceptive pill have higher preference towards men with genetically similar MHCs.

This interruption in a woman’s natural attraction towards genetically different men as a result of the use of contraceptive pills will contribute to difficulties while trying to conceive as well as increased risk of miscarriage during pregnancy. Besides that, a child’s immune system will also be weakened due to lack of diverse genes being passed down.

"Generally, the findings show that oral contraceptives can influence a woman's MHC preference,” said Roberts. However, it is not apparent that hormones in contraceptive pills can directly affect a women's sense of smell as the control women in the study showed no MHC preference.

Therefore, it is concluded that besides leading to fertility problems in MHC-similarity couples, breakdown of relationships often occur when women stop using contraceptive pills. This is due to the fact that odour perception remained as one of the essential aspect at maintaining attraction to partners.

Despite a psychologist at the University of New Mexico in Albuquerque, Steven Gangestad who found the results of the study to be "intriguing", this area of research is worth to be venture on in the future to provide stronger association between the use of contraceptive pills to women’s choice of partner.

References:
http://www.sciencedaily.com/releases/2008/08/080812213824.htm
http://sciencenow.sciencemag.org/cgi/content/full/2008/813/4

41550629

Functional Genomics of Rice

2008-10-07T00:12:00.002+10:00

Rice is consumed by nearly half of the world’s population and considered as the staple food for the largest number of people on the earth. Over the past 40 years, there is about 2.3 fold increase in rice production. This is largely contributed by intensive research leading to better varieties that showing higher growth rate, yield potential as well as resistance towards pests, disease and abiotics stresses.

Functional genomics is a field of molecular biology that attempts to make use of vast data produced by genomics projects to explain and describe gene functions and interactions. Unlike genomics, functional genomics concentrates on dynamic aspects such as gene transcription, translation and protein-protein interactions rather than the static aspects of genomic information such as DNA sequences and structures. To produce high yielding varieties of rice suited to specific locations, functional genomics of rice is essential to understand fundamental yield-limiting factors at molecular level to help deployment of natural and engineered genetic variability most effectively.

Success in genome sequencing is paving the way for preparing a road map of functional genomics, which is expected to correlate action of a gene to a trait in cellular and organism context. Realizing the immense potential, various nations have provided huge in-put to researchers to initiate investigation on functional genomics of plants. This includes analysis of expression profiles, generation of mutants and tagged lines or target-specific silencing of genes, functional validation in transgenics, allele mining, comparative genomics and virtual plant concept. It is estimated that the rice genome may contain 37,544 genes. Functional analysis of these genes and their useful alleles would be a challenge for rice scientists in near future and require global attention and initiatives by various countries.

Source: http://www.genomeindia.org/rice/functional/about.html

Christopher Lee (41815467)

Viruses: A lethal taste of water

2008-10-06T21:37:00.003+10:00

We all know what it’s like to get a horrible virus that keeps us away from the enjoyments of university life. Despite feeling like life is over and that the doctors are no help, we have the resources, medications and soft, comfortable beds which aid our recovery thanks to the phenomenal medical advances. Unfortunately, there are many diseases in the animal kingdom that are poorly characterised and for which treatment is but a fantasy.
Thousands upon thousands of marine mammals, from seals and manatees to dolphins and porpoises, have been lost due to unknown variations on the potentially lethal disease, morbillivirus. In 2002, more than 22,000 seals in northern European waters died due to an outbreak of phocine distemper virus, only classified in 1988. We don't even know how it is spread. Does it simply flow on the current or through droplets in the air? Fortunately, the virus isolations, porpoise morbillivirus (PMV) and dolphin morbillivirus (DMV) have allowed for analysis to be started.
Banyard, Grant, Romero and Barrett undertook a study providing comparisons between the variations of morbillivirus at a genetic level. They determined that the morbillivirus genome contains a single strand of negative sense RNA that encodes transcription units that encode structural proteins. One of these proteins is the nucleocapsid protein which has 523 amino acid residues and interacts with both viral and cellular proteins. It plays a vital role in the efficient replication and transcription in the virion and infected cells. Banyard et. al. determined the entire nucleocapsid gene sequence of PMV and compared it with the N gene of all the other morbilliviruses.
The process undertaken saw lymphoblastoid cells infected with PMV derived from a harbour porpoise. Cellular RNA was extracted and subject to reverse transcription forming PCR products spanning the entire N gene. These fragments were sequenced and assembled before being read to ensure that the true PMV sequence was derived. An N protein line-up was generated using other morbillivirus sequences retrieved from the NCBI database. Comparisons showed that PMV and DMV had a high sequence identity with several regions of high conservation in the genome promoter. The antigenome promoters had a greater degree of sequence divergence and varying lengths. There was only two residues difference in the C-terminal fragment and a similar length to all morbilliviruses of 107 nucleotides. A series of hexamer motifs span the untranslated region.
The conclusion drawn was that PMV and DMV do in fact originate from the same virus as they have many similarities in the N gene sequence. Due to ethical and practical constraints, experiments on host species cannot be performed inhibiting the establishment of the route of transmission, the pathogenicity, the host range and global distribution of the disease. Current development of PCR assays to detect and distinguish between the different cetacean morbilliviruses provides hope that one day, this virus genus will be better understood and preventive measures can be enforced to save thousands of marine mammals.

Reference: Banyard, AC et al. Seuqence of the nucleocapsid gene and genome and antigenome promoters for an isolateof porpoise morbillivirus. Virus Research 132 (2008) 213-219

Alana Evans (41806438)

‘No entry’ to HIV cells

2008-10-06T15:42:00.002+10:00

In case you are wondering, yes, we are talking about stopping HIV virus infection. HIV tends to infect certain cells when they are inside our body. Experiments done on mice showed that mice are capable of becoming resistant to HIV virus by damaging a gene in one of the blood cells that HIV infects which are T-cells.

Mice are able to change their gene so that T-cells cannot make CCR5, a surface protein onto which HIV virus hooks on before entering the cells. The virus thus cannot infect the cells anymore.

The researchers at Sangamo BioSciences, a biotechnology company in Duarte, California, US, make amendments to the gene by inserting zinc-finger nuclease into the cells. The zinc-finger part cuts only a specific part on CCR5 gene which is then nicked open and altered by the nuclease part. This change to the cells is permanent, said Elena Perez from the Children’s Hospital of Philadelphia in Pennsylvania, one of the collaborators of this study.

In one of the experiments, half of the mice are given human T-cells treated with the zinc-finger nucleases, and the other half given untreated T-cells. After that, the mice were infected with HIV. It is found that mice given zinc-finger nucleases are resistant to HIV.

The Sangamo hopes to extract T-cells from patients with HIV virus and alters them so that they will not make CCR5 protein when placed back into the bloodstream. As the altered cells multiply in the body, the researchers hope that they will become dominant and thus give longer protection to patients compared to drugs that can block CCR5 molecules.

Is this permanent change? Maybe there is really hope that we can cure HIV patients if the daughter T-cells with altered CCR5 gene dominate the T-cells in the body. The Sangamo hopes to test this treatment in patients by the end of this year.

41550973

Reference:
HIV 'locked out' of sabotaged cells,

Watch Your Laughter - It's Gene Related

2008-10-04T18:40:00.012+10:00

Did you know that gene expressions are closely linked even to our everyday laughter? Recently a team of scientists lead by Dr Takashi Hayashi took experiment to distinguish the effect of laughter and it's possible ability to shift gene expression.

It is known from previous psychological reports that laughter will provide a boost on various human immunological aspects, which proves to be beneficial to the body. Reports prove that negative emotion will elevate blood glucose levels within the body, so therefore when the diabetic patient laughs, which is a sign of positive emotion, Dr Hayashi hypothesised that postprandial blood glucose (PPBG) levels will decrease and will influence the gene expression profiles in the peripheral blood leukocytes.

Dr Hayashi and his team conducted their experiment on in-patients all diagnosed with Type 2 Diabetes and all currently undertaking self-management plans. This allows access to patient records while also monitoring their glucose level changes without any other factors. A cartoon video is shown to the patients and the hospital staff, which they all laughed throughout. Blood samples before, one and a half and four hours after the video is recorded. Another video on diabetic educational program is played for them on the second day and the exact same procedure is taken.

Around 41,000 blood samples from the patient is then determined via microarray technique. Results displayed that laughter up-regulated 39 genes, in which 27 increased its expression throughout and after the comic video period but not the program video. Further functional classification shows that 14 genes were found to be related to the Natural Killer Cell Activity. Although no gene is found to be responsible for glucose level regulation, genes responsible for PPBG supression has been seen.

The results further justified that laughter stimulates immune system response and withstand PPBG elevation through a module of Natural Killer Cell Activity caused by up-regulation of relative genes. Consequtive studies also suggest that laughter will prevent exacerbation of diabetic nephropathy.

Full article can be seen at http://www.jstage.jst.go.jp/article/biomedres/28/6/281/_pdf

41769944

Stopping cancer cells going mad ! -New cancer therapy targetting miRNA

2008-10-04T14:39:00.005+10:00

Potential anti-cancer drug that targets particular genetic regulators responsible for the rapid growth of cancer cells has been discovered by North Carolina State University Chemist.
The gene regulator is known as MicroRNA or miRNA, which can shutdown and prevent expression of genes. Huang, an assistant professor in Wistar's Molecular and Cellular Oncogenesis Program emphasizes the new therapies' selectiveness attributed to the specific target molecule (miRNA), and fewer side effects compared to conventional chemotherapy drugs.
MicroRNAs are small, single-stranded molecules which are about 20 nucleotides long.
They are responsible for the gene translation and more than 30% of gene regulation processes. If miRNAs are over or underrepresented, genes are over or under expressed, possibly leading to cancer.
Researchers focused on specific miRNA called miRNA-21, which makes cancer cells anti-apoptotic (prevents cell death) in glioblastoma which contributes 52% of the total brain tumors. Hence, by lowering the miRNA-21 level, it is possible to induce cancer cell death.
Deiters and colleagues have discovered a molecule that reduces the level of miRNA-21 by 80% after testing 1,200 separate compounds, which probably works by preventing the miRNA-21 from being transcribed.
This potential drug does not kill the cancer cells directly, but makes cancer cells susceptible to conventional cancer therapy as the cells are not anti-apoptotic anymore.

By Ji Wung, Bang (41590782)

Source article:
http://www.sciencedaily.com/releases/2008/09/080924184657.htm

Progress in Gene Tailored Therapeutics

2008-10-02T19:35:00.003+10:00

Genes are constantly being discovered, those for individual characteristics such as alcohol tolerance or rose pigmentation and some for conditions such as insomnia. But what do these known genes amount to? One of the most important and practical association made with genes is their linkage to certain conditions. Many have considered tailored therapeutics based on genomic make up but researchers at the Centre for Applied Genomics in the Children’s Hospital of Philadelphia are putting it into practice. Since 2006 they have been making an effort in genotyping, the process by which allelic variations are attributed to a condition.

By processing large amount of genomic sequences in their vast database patient blood samples the organisation aims to recover links between certain common ailments and particular genes. Using the genes and knowing their contribution to certain diseases enables a better understanding and treatment of them. Genetic profiles are also constructed for patients, which can be used to both accurately diagnose and properly target treatments. Additionally there are plans to develop broader ranged therapeutics with biopharmaceutical companies to treat not only those with a particular allele but all individuals without a gene variant ho have the disease.

The division at the Children’s Hospital of Philadelphia currently is able to analyse 550,000 various copies of a gene from 264 patients in one day. Soon they will become the largest genotyping project in the world with the potential to examine 150 million genotypes per day. As Dr. Hakonarson the leader of the Centre for Applied Genomics, comments, "We will be able to characterize genotypes and health conditions over a sizable population of children. This project will help to set the standard for identifying biological links to childhood diseases."

More recently, Dr. Hakonarson in his 7th July publication said it was already now possible to link gene variants with complex disease, such as age-related macular degeneration, Type 2 diabetes, inflammatory bowel disease, obesity, autism and leukemia. Later in a paper published in Nature on the 2nd of August his team had found one of the genes responsible for type 1 diabetes. These gene recognitions are stepping stones on the future Dr Hakonarson envisioned. A couple decades from now you could skip the symptoms and just give your local GP your genome!

By: Michael Chen 41746561

Main Source: http://www.bio-medicine.org/biology-news/Large-scale-genomics-project-will-hunt-genes-behind-common-childhood-diseases-3511-1/

References:
Hakonarson H, Grant SF, Bradfield JP, Marchand L, Kim CE, Glessner JT, et al. A genome-wide association study identifies KIAA0350 as a type 1 diabetes gene. Nature. 2007 Aug 2;448(7153):591-4. Epub 2007 Jul 15.

Grant SF, Hakonarson H. Recent development in pharmacogenomics: from candidate genes to genome-wide association studies. Expert Rev Mol Diagn. 2007 Jul;7(4):371-93.

For more information visit the site for the Children’s Hospital of Philadelphia, Center for Applied Genomics Division, http://www.chop.edu/consumer/jsp/division/generic.jsp?id=84930