Genetically Modified Tomatoes May Help Prevent Cancer…

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.

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.

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

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

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?

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

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

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

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?

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

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!

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?

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

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

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

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

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

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

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

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