The Beauty of Symmetry

A recent study has suggested that the expression of a single gene in mice is crucial to the prevention of errors during neuroepithelial stem cell division, which subsequently prevents the formation of asymmetrical daughter stem cells. Scientists envisage that this new genetic discovery may allow an insight into possible treatment of several brain disorders in humans including lissencephaly (‘smooth brain’ disease), to be obtained.

Previous studies have illustrated the importance of the LIS1 gene, (the human equivalent of the mouse gene under scrutiny), in the migration of nerve cells from the cerebral cortex. The absence of the two copies of the LIS1 gene in humans causes the nerve cells in the developing brain to function improperly, resulting in a thick layer of nerve tissue, associated with lissencephaly.

A report published in the Feb. 8 Edition of The Cell, by the Institute for Human Genetics at the University of California, suggests that the importance of the LIS1 gene is not merely confined to nerve cell migration in the brain. The study, which involved the expression and suppression of the LIS1 equivalent gene in embryonic mice during different stages of their embryonic development, yielded unexpected results. The findings suggest that the expression of the LIS1 equivalent gene in mice during embryonic brain development is also critical to the mitotic phase of the neuroepithelial stem cells.

More specifically, the expression of the gene was shown to monitor the orientation of the mitotic spindle so that both daughter neuroepithilial cells obtain the correct number of duplicated chromosomes and other cellular components following cytokinesis. The researchers at the Institute for Human Genetics hypothesize that the LIS1 equivalent gene monitors the orientation of the spindle by regulating the movement of a ‘molecular motor’ called dynein. “Just like a pulley, dynein draws the microtubules through it, and that, in turn, rotates (reorientates) the spindle,” senior author, Anthony Wynshaw-Borris, PhD, MD, hypothesizes.

The study also showed that suppression of the gene results in the spindle being unable to rotate properly, which impairs its ability to undergo symmetrical mitotic division. Asymmetrical division of neuroepitithial stem cells during the early stages of embryonic brain development greatly impairs the function of the neuroepithelial cells and consequently affects other embryonic developmental processes. Neuroepithelial stem cells are the derivatives both glial progenitor cells and nerve cells, so impaired functioning of these stem cells will also affect its derived cells.

One now poses the question as to whether the asymmetrical division of neuroepithelial daughter cells is the cause of some of the rarest and most severe brain disorders. If so, will the expression of the LIS1 gene in humans provide a breakthrough treatment?

To view the original article: www.medicalnewstoday.com/articles/101900.php

Further Resources:
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B8G3V-4S098WF-3&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=0cf3a02f27c7fa63c6a69b1df6292500.

http://www.ncbi.nlm.nih.gov/pubmed/9039800

http://en.wikipedia.org/wiki/Neuroepitheliomatous
By Peter Bell

One-Minute Mapping

Nanotech News
July 18, 2005
One-Minute Mapping
Restriction mapping is a widely used technique in molecular biology for identifying gene mutations. Now, a research team led by Robert Austin, Ph.D., of Princeton University has created a microfluidic device that can perform restriction mapping in less than a minute on single DNA molecules. The investigators believe that this technique, which is reported in the journal Proceedings of the National Academy of Science USA, can also be used to study how certain enzymes interact with DNA.

Restriction mapping uses so-called restriction enzymes that recognize and cut DNA at specific sequences, known as “restriction sites,” producing well-defined DNA fragments. Each of the many commercially available restriction enzymes are capable of cutting DNA at a specific sequence, or order, of nucleotide bases (A,T,G and C) within the millions of bases in a piece of DNA. Most often, each restriction enzyme will find several of its particular restriction sites within a piece of DNA and will produce a series of fragments that can be easily separated by their length. When a mutation occurs within a restriction site, the corresponding restriction enzyme no longer recognizes that site and the resulting pattern of fragments changes, producing one longer rather than two shorter fragments for each missing restriction site. Restriction enzymes require magnesium ions to function, which turns out to be a property that the Princeton team took advantage of in constructing their device.
The key to restriction mapping on a microfluidic device is the ability to first stretch a piece of DNA within a nanoscale channel so that restriction enzymes can then find their corresponding restriction sites and cut the DNA molecule. The investigators accomplish this feat by constructing parallel channels 100 to 200 nanometers in diameter on polished quartz wafers and connecting them with a series of smaller channels running perpendicular between the two larger channels. The ends of each of the two larger channels were connected to electrodes, producing a system that can move DNA into and out of one of the two larger channels and magnesium ions into and out of the other of the two larger channels.

Preparing a restriction map starts when both of the two larger channels are loaded with a restriction enzyme. The electrodes are powered so that DNA moves into one channel and magnesium ions stay in the other channel. Restriction enzymes will quickly bind to the DNA molecule so that by the time it is fully stretched within the channel, the enzymes are ready to do their cutting. At this point, the voltage applied to the electrodes is changed so that magnesium ions flow into the DNA-containing channel, which enables the restriction enzymes to slice DNA into its expected fragments. The lengths of these fragments are easily measured using an optical microscope as they exit the device. This work is detailed in a paper titled, “Restriction mapping in nanofluidic devices.” A reprint of this paper is available at no cost at the journal’s website.View paper.


Posted by s4175728 - Colby Hart

Modified Sorghum to Boost Nutrition in Africa

Researches from Pioneer Hi-Bred International Inc. are helping develop a transgenic sorghum that will be more nutritious for the 300 million Africans who relied on grain to comprise the majority of their diet. Sorghum is an important crop due to its ability to grow in arid environments where irrigation is not accessible or affordable. However it lacks essential nutrients and is not easily digestable. As a part of the Africa Biofortified Sorghum Program the aim is to produce grain suited to the harsh climate which benefits consumers. This entails developing sorghum with more vitamin A and E, available iron and zinc and easily digestible essential amino acids.

Despite these potential benefits genetically modified crops is controversial in Africa. As it is a developing country the primary concerns include the threat to their biodiversity, traditional food crops, production systems and native culture. As a result researches have been unsuccessfully in securing permits to conduct trials in South Africa. Even if production is approved, another problem facing the genetically modified sorghum is that a distribution system is needed to ensure seeds reach the hands of low-resource farmers. Potentially this product could enhance the nutritional health of millions, however there are many barriers that must be overcome before such results become apparent.

Further Reading

http://supersorghum.org/project.htm
http://techafric.blogspot.com/2007/09/africa-biofortified-sorghum-abs.html

Blog Based on - Perkins, J 2008 ‘Modified Sorghum to Boost Nutrition in Africa’ Australian Grain, Jan – Feb, Volume 17 no.5, p.5

Posted By: Chloe English
Student #: 41732975

Bipolar in a Cup

Home diagnosis test are not considered a novel notion within today’s society. However, with rapid scientific developments many genetic tests have become available which claim to assist with the prediction of a wide variety of illness and even cancer. Last month Dr. John Kelsoe, a geneticist at the University of California, began offering and supplying one of the first psychiatric gene tests.

Dr. John Kelsoe and his company, La Jolla based Psynomics, have designed and produced a test which allows the public to test their individual susceptibility to developing bipolar based upon their genetic make-up. The bipolar genetic tests began Internet sales last month at a price of $399. The test simply requires the patient to spit into a cup which they are sent by mail. The cup is then returned to Psynomics where the DNA is analysed.

Kelsoe’s decision to release the test to the public follows his career research into determining the biological roots of bipolar disorder. He admits that his research on the genetic basis of the illness still remains incomplete. However, Kelsoe and Psynomics are suggesting that the test be used as a diagnostic tool rather than a way to successfully predict a person’s risk of developing bipolar later in their life. Despite the presence of genetic variations which sometimes suggest future development of the disease, Kelsoe admits that the disorder probably occurs as a result of both life experiences as well as such genetic variations.

The release of these gene tests onto the market has sparked debate and split public opinion. Many health experts are concerned that products such as the bipolar test are increasing the anxieties of the public. As well as this, there is continued concern that the public does not have enough understanding of the condition in order to interpret the results correctly. Whilst some who discover the presence of bipolar related gene variations within their DNA may never actually develop the condition, it is still possible that people who receive negative results could still develop bipolar.

The test is yet to establish any strong validity, something that should have been established before the “$399 spit cup” was sold to the public via the easily accessed Internet. Although the test may legitimately provide a fast and efficient way of diagnosis in the future, at present the process requires all patients to be better educated. The public need to be better informed not only to understand the results and the implications of these results, but simply the condition itself.

For further information: http://ap.google.com/article/ALeqM5hlqjYlBDA0tRjKUb6V_EfK3UuccAD8VIMMNGo

Image: Dr John Kelsoe and his colleagues

http://media3.washingtonpost.com/wp-dyn/content/photo/2008/03/22/PH2008032201541.jpg

Posted by Jess Lister (41760848)

Happy genes !

According to researchers from the University of Edinburgh and the Queensland Institute of Medical Research in Brisbane, they have found that our personalities and happiness are largely hereditary and the genetically-determined personality traits affect our happiness.

The research, published in the latest issue of the journal Psychological Science, rated the personalities of 973 pairs of twins. In the research, a Five Factor Model of personality is used to rate the twins in which measures neuroticism, extroversion, conscientiousness, openness and agreeableness. The study shows identical twins have a very similar personality and wellbeing. But fraternal twins are only around half as similar. Hence, this suggests that genes are responsible for certain personality traits.

Those who are conscientious, extroverted and not overly neurotic are more likely to be happy and people with these personality traits tend to have a happiness 'buffer' to help them through hard times. While the researchers found happiness has its roots in our genes, half is related to our work, health or relationships.

One of the researchers Professor Timothy Bates says this research is the beginnings of a new theory of happiness. "It helps us understand what was otherwise a real puzzle. Why do people tend to show stable differences in happiness? It turns out that if we want to understand happiness, we will need to understand personality," he says. He also comments that personality traits of being outgoing, calm, and reliable are it 'affective reserve' that drives future happiness.

Professor Robert Cummins, from the Australian Centre on Quality of Life at Deakin University in Melbourne, says it's in our best interests to be positive and personality has a 'set point' around which we maintain our wellbeing. "The average person feels well satisfied with themselves and their life and that's the average set point ... even people with low set points feel positive. Besides remaining positive in your outlook is incredibly important, it gives you a motivation for doing something when you wake up in the morning and makes you get on with life and do things " he says.

Bates says the latest research confirms most us are happy for much of the time, that we generally like who we are and we don't want to change too much. Although he says the study could shed some light on mood disorders such as depression. "Linking happiness to personality and a focus on the positive will help our research into therapies and ways to avoid the low end of the happiness [scale] - depression."


Resource :
http://www.abc.net.au/science/articles/2008/03/06/2182127.htm?site=catalyst&topic=human

Further Readings :
Psychological Science, March 2008, Vol. 19 Issue 3 Page 205-210, Happiness Is a Personal(ity) Thing: The Genetics of Personality and Well-Being in a Representative Sample, Alexander Weiss, Timothy C. Bates, and Michelle Luciano

The search for our selfish gene

Through evolutionary biology we have come to believe that every animal is born to be selfish in order to survive, adapt and breed. ‘A predominant quality to be expected in a successful gene is ruthless selfishness,’ (Dawkins, 1976). Cognitive and evolutionary psychologists have formulated their own ideas as to why humans are selfish and what drives the selfish desires or traits of an individual. Recent research has lead to the possibility that we are born that way.









For the first few years of a regular child’s life they are primarily selfish, some continue this trait all through life. A newly born baby doesn’t care for others, only for its own hunger, fatigue or boredom. Researchers have claimed that there is sufficient evidence to believe that there is a gene containing the material that drives our selfishness. The ‘selfish gene’ has not yet been found. This gene is the basis for our morals, which develop with age and influence. Combine the gene our morals and emotion and you have all the tools necessary to make a cooperative or selfish choice.



At the moment the focus is on finding if the selfish gene actually exists. Philosophical speculation as to what it will mean if the gene is found is well in discussion. If we are born selfish then how did we develop into emotional and moral creatures all those centuries ago? If the gene is discovered it will be a big day for biology but perhaps more of a focal topic in philosophical circles.





by Michael Milevskiy


41736973





Dean, T (2007) Right & Wrong, COSMOS, issue 17, page 46-53, Luna Media



Picture: Dean, T (2007) The Science of Good & Evil, issue 17 October, Luna Media, http://www.cosmosmagazine.com/node/1870 accessed: 28th March 2008

Further Reading: Richard Dawkins, 'The Selfish Gene'
: The Selfish Gene, http://en.wikipedia.org/wiki/The_Selfish_Gene

Aquatic Animals the Answer to DNA protection?

- post by Tom Hockings (4177030)

The freshwater Bdelloid Rotifer

Recently a team of scientists from Harvard University have made detailed studies of the freshwater invertebrates bdelloid rotifers in an attempt to understand their remarkable genetic make-up. Bdelloid rotifers are the most common of freshwater Metazoa that you can find in your pond, but these 0.5 mm organisms are more than they seem. With an ability to live hundreds of years when dried or frozen and the physiology to withstand extreme amounts of gamma radiation, the genetic make-up of these organisms is looking increasingly promising. The main attraction of these little creatures however lies with its extreme genetic resistance to radiation, continuing to reproduce after large doses of gamma radiation, much greater than that tolerated by other any other studied species. http://www.micrographia.com/specbiol/rotife/homebdel/bdel0100.htm#bdellink


The reason this is so important is because the effects of radiation have long been linked to the cause of inflammation, cancer and premature ageing. The hope is that this new study will start off new lines of research into these problems. "They are able to recover and resume normal reproduction after receiving a dose of radiation that shatters their genomes, causing hundreds of DNA double-strand breaks which they are nevertheless able to repair." says Meselson, Thomas Dudley Cabot Professor of the Natural Sciences in Harvard's Faculty of Arts and Sciences. http://www.medicalnewstoday.com/articles/101634.php


This regenerative quality has been deemed interesting enough to further their studies, with the hopeful end product being a way to repair damaged genetic material and DNA strands in our human genome. While the bdelloid rotifers have been studied for nearly over 300 years, they are only finally being understood lately. It has been observed that it’s actually their ability to protect their DNA repairing tools rather than their DNA which is proving to make them so remarkable. Hopefully with further study and research the secrets of this organism will be used to fight cancer and other genetic ailments.

References:

Picture - http://www.micrographia.com/specbiol/rotife/homebdel/bdel0100.htm#bdellink

http://www.medicalnewstoday.com/articles/101634.php

Born with a left wing

It has been well established in the scientific community thus far that an individual’s appearance plays only a part within genetic inheritance. However, many scientists are now proposing that a person’s political stance is also influenced within the individual’s genes.

This outlandish idea is not too farfetched when considering that politics is largely based on personality. Numerous investigations suggest that certain genes are linked to the individuals accepting capacity. James fowler, a political scientist and Ira Carmen, of the University of Illinois individually proposed that the genes; 5HTT and MAOA, and also D4DR respectfully, interact with levels of neurotransmitters in the brain to effect whether a person is ultimately right or left-winged. Democrat MP Matthew Taylor; great-grandson of an MP, agrees, "If I were to guess I would say that I have inherited the characteristics of wanting to get up and argue my case."

This opinion is furthered by a neuroscientist, David Amodio and his 2007 work with mental resistance relating to an individuals genetic habit. The results showed that conservatives had less brain activity then liberals when resisting the habit. Amodio believes this reflects personality traits; care, sociability and openness and thus their political make-up associated with these qualities.

Support for this theory is continuing to emerge with further research such as the study of differing political views between identical and non-identical twins. Dr John Hibbing exposed that the percentage of identical twins giving the same answer significantly outweighed the fraternal twins’ correlation, "What we are trying to establish is whether people who share some similar characteristics in their DNA also share a particular political trait." Hibbing deduced that the political views would therefore be imprinted in their genes.

This research is proving controversial within the scientific community with many proposing that political stance is largely indoctrinated. Hibbing agrees to an extent, "We still say that at least half of our political beliefs are still influenced by our environment."

Posted by: Bianca Gormley

To view full articles:

http://www.newscientist.com/channel/being-human/mg19726411.800-are-political-leanings-all-in-the-genes.html

http://news.bbc.co.uk/1/hi/magazine/7315656.stm

Image reference:

http://news.bbc.co.uk/1/hi/magazine/7315656.stm

Flourescent Felines: The Pet of the Future?

A team of South Korean scientists at the Gyeongsang National University have succeeded in what could appear to be the strangest genetic modification ever.

The research team led by Kong Il-keun have acchieved a world first when they cloned the first cats with modified genes ever, in an effort to treat diseases in animals as well as the close to 250 diseases that human suffer that bare similarity to feline illnesses, with one small hitch, the new GM kittens glow red when they are placed under UV light.

The cats were modified by the addition of a red fluorescence protein to the skin tissue, which causes the tissue to, when viewed under ultraviolet light, appear red. The modified skin cells were then fused with an egg cell without a nucleus; the result - two Turkish Angoras that may be the next step in the treatment of human and animal genetic diseases.

However, the discovery has not come without it's fair share of debate, mostly over the success rate with regards to genetically modified and cloned creatures, raising the same theological and ethical questions that have been asked for many years. Though while these questions of ethics have and will continue for many years, it seems that for now we may have not only a new kind of pet, but a novel solution when it comes to home lighting.

Posted by Ben Sandford

For more information go to:

http://english.chosun.com/w21data/html/news/200712/200712130008.html

http://www.escapistmagazine.com/articles/view/issues/issue_141/3029-Weird-Science.2

http://www.abc.net.au/news/stories/2007/12/13/2117451.htm

http://inventorspot.com/articles/scientists_create_glowinthedark__9191

Bacteria in Oceans Used in the Fight Against Cancer

Posted by Sahan Bandara (41777556)

Scientists at the UCSD’s Scripps Oceanographic Centre for Marine Biotechnology have discovered an ocean-inhabiting culture of bacteria that can be used in the fight against a cancer. Salinispora Tropica was discovered in ocean sediment off the coast of Bahamas in 1991, but scientists have only now unlocked the genomic sequence of the organism, which in turn has revealed its cancer-fighting attributes.

Essentially, Salinispora Tropica’s anti-cancer potency lies in one of the enzymes it produces, known as Salinosporamide A. In a nutshell, Salinosporamide A, like a number of other anti-cancer drugs, fights cancer by inhibiting proteasome activity by modifying the active site of the 20S proteasome.

In the past, scientists have had to artificially incorporate chlorine into a number of anti-cancer drugs to make it more effective. However, this particular enzyme has the natural ability to incorporate chlorine atoms. The chlorine atom in Salinosporamide A makes the enzyme’s binding to its biological target irreversible, which explains why this substance is more effective in fighting cancer than some of the other cancer treatments.

This naturally occurring enzyme is believed to be five hundred times more effective than its chlorine-free contemporary, Salinosporamide B. Consequently, Salinosporamide A is already being clinically trialled for the treatment of multiple myeloma, a form of cancer that affects plasma cells. The discovery of Salinispora Trpoica may also aid scientists in better understanding evolutionary developments in bacteria and why similar enzymes are activated in dissimilar ways.

Further Reading:
http://www.associatedcontent.com/article/526461/new_potent_cancerfighting_marine_product.html
http://www.news-medical.net/?id=34016

Fruit Fly Gene From 'Out Of Nowhere'

The new gene, called hydra, exists in only a small number of Drosophila fruit flies. It suggests that it was created about 13 million years ago. And early evidence indicates that the new gene is functional (as opposed to being nonfunctional "junk" DNA) and is likely to express a protein involved in late stages of sperm cell development (spermatogenesis).

The general idea was that new genes were always formed from tinkering with other genes, but there is no homologues [genes with a similar structure] in this gene. Any similar or related gene with the hydra has not been found yet. That is what hydra makes itself unique.

Hsiao-Pei Yang, a senior research associate in Cornell's Department of Molecular Biology and Genetics and senior author of a paper published in the July 6 issue of the online journal PLoS Genetics (Public Library of Science Genetics) conducted part of this research while at the National Yang-Ming University in Taiwan and part of the work in collaboration with Cornell's Daniel Barbash, assistant professor of molecular biology and genetics.

It has not yet been found out that how the hydra gene was created, but researchers assume that the gene may have developed from a piece of DNA junk called a transposable element (also known as a "jumping gene"), which might have been inserted into the genome by a virus. These transposons can copy and insert themselves into DNA sequences. For example, one theory is that when a transposon sits next to a gene and then jumps to a new location, it carries part of the gene sequence it was next to and inserts it in the new location. Often, transposable elements appear to have no function or may be harmful and are eliminated by natural selection, but researchers are beginning to think transposons may be a source for creating new functional genes as well. The hydra gene is named after the Greek mythological beast that had a hound's body and nine snake heads, because it has nine duplicated first exons (sections of the gene that contain protein-coding information). Each of these exons may serve as alternative starting positions for the gene to become activated. The researchers found that most of these exons had a sequence for a transposable element sitting right next to it. Duplicated sequences generated by transposons may be part of the mechanism for creating new genes, as the duplications provide more chances for a gene to evolve.

For more information

http://www.sciencedaily.com/releases/2007/07/070723160028.htm

posted by Taihei Sakaushi
Student number 41283244

Breast Cancer ‘Master Gene’ Found

Scientists in America had identified a key gene, which cause to the spread of breast cancer tumor to other parts of the body. This finding can be lead to the development of drugs to cure the patients with breast cancer.

Breast cancer is the second most common cancer type, after lung cancer, and it is the fifth most common cause of cancer death. It can occur both in men and women, however, it is really rare that a man to have it. Among women, breast cancer is the most common type of cancer, both in incidence and death. Estimated new incidences of breast cancer in United States in 2008 is 184,450 and estimated death from it is 40,930.

The scientists found that a gene called SATB1 is expressed in breast cancer sells, and it controls around 1,000 other genes in tumor cells, which facilitates the spread of cancer cells.

SATB1 is a nuclear protein, and it is well known as a very important master gene in immune system, as it takes crucial role in regulating gene expression during differentiation and activation of T-cells. In this research, it is discovered that this master gene has a cause to spreading breast cancer tumor.

When STAB1 is over activated, it results to the numerous other genes to promote metastasis. The researchers found that when SATB1 is present in a breast tumor, there is high possibility that the cancer will progress or recur. In addition to this, it is found that when SATB1 is introduced into non metastatic breast cancer cells in mice, it can induce invasive cancer tumors. The interesting point is that the opposite way of this reaction was also been observed that taking SATB1 away from metastatic cells not only stop metastasis and tumor growth in mice, but it also returns cells to their normal appearances.

This discovery of the gene SATB1 becoming the key cause in aggressive breast cancer can be lead to the development of new treatment for the breast cancer in the future.

For more information,

http://news.nabou.com/sci-tech/genetics_news.html

http://www.news-medical.net/?id=36201

Mai Ota 4160068

Frog Skin May Cure Diabetes Sufferers

A South American Nocturnal frog may prove to be the key to solving the type 2 diabetes puzzle. The Pseudis paradoxa (Paradoxical Frog) got its name due to its strange ability to shrink as it matures. However, scientists studying its skin have discovered that the paradoxical frog has another uncanny ability. It has recently been revealed that the frog’s slimy skin contains a particular compound that can stimulate the release of insulin, the fundamental hormone that is lacking in diabetes sufferers.

So far, scientists have reproduced an artificial copy of the peptide (known as pseudin-2), a protein building-block that protects the paradoxical frog from disease. Researchers have suggested that this peptide could be used to increase insulin production in people with type 2 diabetes.

Researchers from the University of Ulster and United Arab Emirates University have tested the artificial copy of the peptide and found that it increased the release of insulin in cultured cells by 50 per cent. They believe that the synthetic version could join a new class of medicines, which would highly advantage diabetics by helping them control their condition when other forms of treatment have failed. With these discoveries, the future does indeed look brighter for diabetics.

By: Student Number 41756328

for more information go to

Full Article: "Amazon frog may help battle type-2 diabetes." "The Australian" March 4 2008

http://www.abc.net.au/news/stories/2008/03/04/2178827.htm

'C' the Overhang:

Posted by Adam O’Donoghue, student No # 41719350

An interesting study was performed at the Salk Institute for Biological Studies by Associate Professor Jan Karlseder on the chromosomal structure of the roundworm C. elegans. The study examined telomere formation at the ends of chromosomes, and their possible role in the formation of cancer cells. Most animals protect their chromosomes with terminal DNA sequence overhangs rich in the base guanine (G). The roundworms, however, were found to be able to form another protective overhang, one rich in the base cytosine (C).

Karlseder, in an article published by “Science Daily”, commented on his team’s findings, saying that they were very unexpected. “Telomeres protect the ends of chromosomes like a glove” he stated. “In mammals, telomeres have a single stranded overhang with a ‘TTAGGG’ sequence about 150 bases long. We found that in worms there can also be a single-stranded overhang of a C-containing strand”.

The formation of telomeres on chromosomes is an essential part in DNA replication and mitosis, and is necessary in all animal cells. Telomeres deteriorate with age and are associated with cellular senescence, abnormal growth and death. Karlseder explains: “Telomere loss can lead to chromosome fusion, if that happens when a cell divides, its chromosomes could randomly join and break, leading to a condition know as ‘genome instability’, a major cause of cancer”.

The study found that the G- and C-tails uniquely connected to a particular side of the DNA molecule. G-tails extended from the 5’ end, and C-tails from the 3’ end. It was also discovered that two unique proteins in the worm bound preferentially to the C or G overhangs, thus affecting the length of the telomeres and possibly influencing the cells bio-clock.

The significance and scope of the findings remain to be determined by comparable studies on other animal species. Karlseder noted that “C. elegans is an established model to studying age, We can screen the whole worm genome relatively cheaply in a few months. The same experiment in human cells would take years and probably ten times the money. We want to exploit the C. elegans system and then translate our findings into a human system.”

However, more research is needed to actually determine whether the C-tails are unique to worms or have just been overlooked within mammals. “It’s premature to think that C-tails do not exist in human cells. We may find them in mammalian cells under certain circumstances, and if so, they could play a role in telomere maintenance and in cancer.”

The study has potential applications in many different areas of research, including the development of possible cancer therapies involving differentially blocking telomere synthesis in cancer cells to curtail cell division. Such applications remain speculative until more detailed studies are conducted to determine the molecular processes involved in telomere formation and function.

‘C’ the overhang: Chromosomal telomeres in roundworms C. elegans

Posted by Adam O'Donoghue, Student No # 41719350

An interesting study was performed at the Salk Institute for Biological Studies by Associate Professor Jan Karlseder on the chromosomal structure of the roundworm C. elegans. The study examined telomere formation at the ends of chromosomes, and their possible role in the formation of cancer cells. Most animals protect their chromosomes with terminal DNA sequence overhangs rich in the base guanine (G). The roundworms, however, were found to be able to form another protective overhang, one rich in the base cytosine (C).

Karlseder, in an article published by “Science Daily”, commented on his team’s findings, saying that they were very unexpected. “Telomeres protect the ends of chromosomes like a glove” he stated. “In mammals, telomeres have a single stranded overhang with a ‘TTAGGG’ sequence about 150 bases long. We found that in worms there can also be a single-stranded overhang of a C-containing strand”.

The formation of telomeres on chromosomes is an essential part in DNA replication and mitosis, and is necessary in all animal cells. Telomeres deteriorate with age and are associated with cellular senescence, abnormal growth and death. Karlseder explains: “Telomere loss can lead to chromosome fusion, if that happens when a cell divides, its chromosomes could randomly join and break, leading to a condition know as ‘genome instability’, a major cause of cancer”.


The study found that the G- and C-tails uniquely connected to a particular side of the DNA molecule. G-tails extended from the 5’ end, and C-tails from the 3’ end. It was also discovered that two unique proteins in the worm bound preferentially to the C or G overhangs, thus affecting the length of the telomeres and possibly influencing the cells bio-clock.

The significance and scope of the findings remain to be determined by comparable studies on other animal species. Karlseder noted that “C. elegans is an established model to studying age, We can screen the whole worm genome relatively cheaply in a few months. The same experiment in human cells would take years and probably ten times the money. We want to exploit the C. elegans system and then translate our findings into a human system.”


However, more research is needed to actually determine whether the C-tails are unique to worms or have just been overlooked within mammals. “It’s premature to think that C-tails do not exist in human cells. We may find them in mammalian cells under certain circumstances, and if so, they could play a role in telomere maintenance and in cancer.”

The study has potential applications in many different areas of research, including the development of possible cancer therapies involving differentially blocking telomere synthesis in cancer cells to curtail cell division. Such applications remain speculative until more detailed studies are conducted to determine the molecular processes involved in telomere formation and function.

The Cost of Genes

$AU56, 000 is the amount a man is willing to pay to potentially prolong his success with bull-fighting (SMH Mar 2, 2008). In March 2009, Victoriano del Rio will be the first Spaniard to be in possession of a cloned fighting bull (Yahoo News, Feb 23, 2008).

Stem cells extracted from del Rio’s stud Alcalde will be sent to genetics firm Viagen in Texas, where the embryo will be produced (SMH Mar 2, 2008).

So what would inspire a man to spend such a large quantity of money on a single bull's genes? Simply; more money. Alcalde has substantially benefitted his master financially through his performance in the bull ring with his "brave style, outstanding horns, good fighting attitude" (del Rio, March 2nd). This Spaniard isn’t alone in this respect however. Viagen claims to have genetically replicated 300 animals, many of which being successful bulls of US rodeos (Yahoo News, Feb 23, 2008).

So in the twenty-first century we’ve effectively reached a point where the quintessentially natural process of reproduction is being controversially exploited for material gain.

16-year-old Alcalde, left.

Picture: Reuters (SMH Mar 2, 2008)

For further reading...

http://www.smh.com.au/news/world/spaniard-wants-to-clone-his-bull/2008/03/02/1204402260678.html

http://www.truveo.com/Load-of-bull/id/2735542421

http://au.news.yahoo.com/080222/19/15xfn.html
Written by Sebastian Whittle

Why the Flu is Worse in Winter

Scientists believe they have discovered why the Flu spreads best during in winter and the reason may lie with a protein laced fatty coating (coloured orange, pictured right) on the virus.

During warmer weather this protein coat stays melted as it travels through the air allowing it to dry out and weakening the virus. However during colder weather the coating hardens protecting it and allowing it a greater chance of survival. The virus must then enter the liquid state in order to infect cells and does so using body heat once breathed in.

It is hoped that this knowledge will lead to more effective ways of fighting the flu.

http://www.livescience.com/health/080303-flu-cold-weather.html

Happy Genes

Did you know that your genes are responsible for your overall sense of happiness and depression?

Scientists have discovered that a change in one “letter” of the gene can have effects on an enzyme that controls levels of the mood chemical serotonin in the brain.

Last year, the scientists discovered an enzyme identified as typtophan hydroxylase-2 (Tph2), which was thought to govern the manufacture of serotonin in the brain.

The scientists found that they had a major impact on the amount of serotonin cells produced when studying the enzyme variants. The results showed that a mouse with one variant produced 50% to 70% less serotonin in its brain than a mouse with the other variant.

"This single genetic difference has a huge impact on serotonin levels, confirming that the gene is fundamental in the synthesis of brain serotonin,” said Dr Zhang.

In other recent studies of genetics in twins, scientists from Scotland and Australia also discovered that genes play a significant part in determining how happy we are in life. “Scientists already knew that subjective wellbeing, or how happy we feel, is linked to personality traits. However, until now, nobody had looked at whether personality and subjective wellbeing had any common genetic origins.”

The study was led by Dr Alexander Weiss, of the University of Edinburgh’s School of Philosophy, Psychology and Language Sciences. Weiss and his colleagues examined 973 pairs of twins, and from the comparisons between the two types of twins (twins with identical genes and different genes), they found that up to 50 per cent of the traits were influenced by genetics. Furthermore, they also pointed out that the other 50 per cent of the differences between people and their happiness can be influenced by relationships, careers and health.

Click on the links to read more about it.

Related Links:

http://www.medicalnewstoday.com/articles/99916.php

http://www.telegraph.co.uk/connected/main.jhtml?xml=/connected/2004/07/14/ecngene14.xml&sSheet=/connected/2004/07/14/ixconn.html

Cellular Rewind <<

Cells on the verge of division (mitotic exit) were once thought to have a pre-destined fate. Cell division was known to be irreversible. However, researchers from the Oklahoma Medical Research Foundation have successfully achieved the impossible, by pushing a cell at mitotic exit back into M phase using chemical agents. Their paper ‘The reversibility of mitotic exit in vertebrate cells’ (Nature, 2006), details this amazing accomplishment.

The mitotic exit stage of cell development is controlled by the breakdown of a type of cyclin, (cyclin B) and also by Cdk1 (cyclin-dependant-kinase 1) inhibitors. By removing both of these factors after the cell had undergone mitotic exit, complete mitosis was reversed, and the cell reverted back to M phase. They observed a re-condensation of chromatids, re-breaking of the nuclear envelope, healing of the cleavage furrow and reformation of microtubules into the mitotic spindle. In most cells, the metaphase plate also reformed, a characteristic feature of a cell in M phase.

This incredible discovery has many future applications, in both research techniques (such as the culture of cells) and in medicine, particularly in anti-cancer drugs. It holds great potential for certain types of cancers where cell division continues uncontrollably, by halting division while still maintaining the integrity of the surrounding cells. This technique would also be able to inhibit the divison of certain groups of cells, which may not be cancerous but which have acquired an unwanted genetic variation.

Still interested?
Check out these links:
http://www.nature.com/nature/journal/v440/n7086/full/nature04652.html

http://news.bbc.co.uk/1/hi/health/4902908.stm

http://www.molecularexpressions.com/cells/fluorescencemitosis/images/mitosisintrofigure1.jpg

Artificial Letters Added to Life’s Alphabet

Two artificial DNA ‘bases’ that can be actively replicated by natural enzymes have been created by US researchers. The addition of two extra bases to the existing 4 bases (cytosine, guanine, adenine, and thymine) will create greater genetic diversity.

Researches hope to in future implement these new bases into the genetic code of living organisms.

These unnatural but functional new base pairs are the fruits of nearly a decades worth of research by chemical biologist Floyd Romesberg, at the Scripps Research Institute, La Jolla, California, USA.

Rosenberg and his colleagues painstakingly created nearly 200 potential new genetic bases each with slight variations on the original bases. Unfortunately these potential bases all failed as their structure and chemistry were not similar enough to the real thing and the polymerase enzymes (the enzymes that replicate DNA inside cells) could not copy them properly.

Frustrated by the slow pace designing and synthesising potential new bases one at a time, Romesberg turned to large scale experiments generating many potential bases at random, which were then screened to see if they would be treated normally by a polymerase enzyme similar to drug development.
With the help of graduate student Aaron Leconte, the group synthesized and screened 3600 candidates. Two different screening approaches turned up the same pair of molecules, called dSICS and dMMO2.

But the team still faced a challenge. The dSICS base paired with itself more readily than with its intended partner, so the group made minor chemical tweaks until the new compounds behaved properly.

Romesberg notes that DNA and RNA are now being used for hundreds of purposes: for example, to build complex shapes, build complex nanostructures, silence disease genes, or even perform calculations. A new, unnatural, base pair could multiply and diversify these applications.

For more info go to
http://www.newscientist.com/channel/life/genetics/dn13252-artificial-letters-added-to-lifes-alphabet.html
Journal of the American Chemical Society

Hydra, the mythical gene

Stephen Huang
http://www.biotechnews.com.au/index.php/id;703620077;fp;4;fpid;1012

Recent discoveries have drawn to light a gene in some fruit flies that has no relation to any known genome. The gene now known as hydra exists only in a small number of species (the melanogaster subgroup) indicating that the gene originated from about 13 millions years ago.

Senior research associate Hsiao-pei yang has stated that this was a ‘de novo “out of nowhere” gene’ because it was thought that ‘new genes were always formed from tinkering with other genes’. However in this case there were no homologues (genes with similar structure) in the fly genome or any species’ genome, making this discovery unique. Evidence found indicated that hydra is a functional gene and is likely to express a protein in the late stages of sperm cell development (spermatogenesis).

The researchers do not know yet how the hydra gene was created, but it has been speculated that the gene may have been created by junk DNA called a transposable element (transposons) or jumping genes that have the ability to move around to different positions within the same genome of a single cell. Transposons have no function and are eliminated by natural selection, but now researchers are beginning to think that they may be a source of creating new functional genes.

The gene was named hydra because of the mythical nine headed monster slain by Hercules. This is in conjunction with the 9 identical exons (any region of DNA that will be represented in mRNA) the gene contains. This is due to the fact that one of the exons had undergone recurrent duplication leading to the formation of these exons. The researchers have also demonstrated that 4 of the duplicate exons can function as an alternative transcription sites. It was also found that 7 of the duplicate exons had a specific transposable element close by. Thus the idea that transposons may have a role in creating new genes was generated.

The Holy Grail of Blood Stem Cells

"The placenta is believed by some communities to have power over the lives of the baby or its parents." Wikipedia



In the light of recent research, this belief is not far from the truth. UCLA stem cell researchers have been working to discover exactly where blood stem cells originate from, in the hopes of being able to mimic this environment and someday help to treat dieseases such as aplastic anemia and leukemia.

Dr. Hanna Mikkola headed up the research team who discovered that it is within the placenta that blood stem cells are generated. Previously, Mikkola and collaborators from Havard and France had seen that there was a large pool of blood stem cells within the placenta, but could not be sure if this was where they had in fact originated, or if they had simply been moved by blood flow from their place of generation. Mikkola's team was able to use a mouse embryo without a heartbeat, and therefore, without blood flow to find that the blood stem cells did infact generate in the placenta. The research was published March 6, 2008 in the journal Cell Stem Cell.

Mikkola's team discovered that blood stem cells are generated in the large arteries of the embryo and placenta. They then move to a niche where they multiply in number and mature. The placenta’s vascular labyrinth (where nutriants and oxygen are tranferred from the mother to the fetus) is the site for this niche.


Red blood cells and a white blood cell

Now that it is known where blood stem cells generate and differentiate into the different types of blood cells (red and white blood cells and platelets)researchers are now closely studying these environments so that they might be able to more naturally coax blood stem cells into differentiating and self-renewing within the lab.


Flow chart of stem cell to differentiated cells

Currently, only by manipulating the cell's nuclear regulatory machinery with genes through the use of retroviruses can blood stem cells be differentiated in the lab. However, as yet, they have been unsuccessful in creating blood stem cells that self-new or do not differentiate prematurely after being transplanted. If researchers are able to study in detail the enviroment in which blood stem cells 'grow up' then they will hopefully be able to have more success in growing blood stem cells in the lab so that in the future, they can be used to treat leukemia and other blood related dieases.

Of late, there have been much success in using human skin cells to create induced pluripotent stem cells (iPS). Coupling this tenquince with the data collected from studying the environments in which blood stem cells mature, could potentially create healthy blood cells for a patient, which are completely immue-compatible with their own bodies. Thus, there would be no cases of graft vs. host disease.

Related Links:

# Blood Stem Cells Originate And Are Nurtured In The Placenta

# Researchers Identify Genes Involved With Blood Stem Cell Development

# Regulating Embryonic Stem Cell Self-renewal

# Researchers Identify Genes Involved With Blood Stem Cell Development

Swiss researchers make telomere discovery

A Swiss Research team from ISREC and the Univerity of Pavia have recently (4/8/07) discovered that Telomeres (1), once understood to be ‘Junk DNA’ with no coding processes and a function that is purely structural, actually have other roles and activities.
Telomeres are the ends of chromosomes in eucaryotes, derived from the Greek ‘Telos’ and ‘Mere’ which literally translates as ‘End Part’. Telomeres do not appear in procaryotes or mitochondrial DNA as they consist of rings and hence, have no ‘end’ as such. Telomeres are DNA which consists of the sequence ‘TTAGGG'(2) in vertebrates, repeated until the physical end of the strand.
Scientists had believed since the 1970’s (3) that telomeres where used chiefly as counting mechanisms for cells and as structural support. These two roles are complementary as the cells require both a structural anchor while they are copied and a mechanism to determine how many times a cell has mitosed. Telomeres serve as a padding and gradually get shorter after the Anaphase in cell mitosis(3). This is to protect the valuable code contain in the DNA and as such many several thousands bases make up the telomeres. Once the limit of the telomeres is reached, the cell dies.
What the Swiss researchers have discovered is that these ‘dead’ ends, do actually take part of reproduction, in that they form RNA copies of themselves(4), which can be used to hypothesize as to why some cells refuse to accept their ‘shelf-life’ as it would seem and become cancerous. It is believed that this new discovery could be applied in the treatment of telomere related tumors.

1 - New Scientist: Chromosome caps may explain cell immortality
2 - Medicine Net; Definition of 'telomere'
3 - Answers.com : Telomeres; Telomere shortening in a long-lived marine bird: Cross-sectional analysis and test of an aging tool
4 - Sciencemag.org : Telomeric Repeat–Containing RNA and RNA Surveillance Factors at Mammalian Chromosome Ends

Gene Mutations have an Impact on Human Longevity

According to a group of scientists, the genes involved with the cell-signalling pathway related to growth also appear to influence the length of human lives. The research centred on those genes involved in the action of insulin-like growth factor (IFG-I) in Ashkenazi Jews aged between 95 and 110.

Animal research had previously shown that mutations to these genes resulted in two effects: impaired growth and longer life spans. Consequently, scientists at the Albert Einstein College of Medicine of Yeshiva University reasoned that the same might hold true for humans.

Research was then conducted on a group of 384 Ashkenazi Jewish centenarians as well as their children. The control group was made up of Ashkenazi Jews the same age as the centenarians’ offspring except with no previous family history of longevity.

The resulting data confirmed the hypothesis. It was found that the daughters of the centenarians were an average of 2.5cm shorter than the female controls and that they were much more likely to have a variety of mutations than were the receptor genes of the controls.

Dr. Barzilai, senior author of the study, has stated that a drug that decreases IGF-I action is currently being tested as a possible cancer treatment and could be used as an age delayer in the future.

For the full story, go to GEN News Highlights.

The actual findings were published in the March 4 issue of the Proceedings of the National Academy of Sciences.

Diabetes cure?

A nocturnal frog found in the amazon may in fact be the answer for millions every year who are diagnosed with diabetes. The Pseudis paradoxa has the ability to shrink as it grows older. This amazing ability is due to a peptide called psuedin-2 which stimulates the release of insulin. Although the research has only just begun, these amazing frogs they have already found so much information.
(Figure 1) A Pseudis paradoxa

It is hypothesized that this peptide could boost insulin numbers for people who have type 2 diabetes. This is very important because this kind of diabetes is prevalent as it is triggered by one's lifestyle and food intake.

Recent tests have shown that in cultured cells this drug has managed to increase insulin production by 50 percent. Another interesting observation about the paradoxical frogs is that the offspring are actually bigger than the parents, with the tadpoles being roughly 27cm and the adults 4cm. Although this discovery is shown to help to produce insulin in cultured cells it still may be a long time before this drug may be available for humans.

Embryo Screening

New Embryo Test:-

British fertility specialists have developed a whole new way to screen embryos for diseases. This means that instead of the previous approximate 200 diseases avaliable for screening, there is now the capabilty to test for almost 6000! This looks like it'll only be for those couples who are undergoing IVF but specialists can now test for inherited diseases for which the specific genetic mutation is not known. With this method, doctors are able to tell whether the baby is a carrier, if it's going to be healthy or not, or if the baby will have the affliction outright. This, however, does bring up the morality issues of discarding embryos because of screening and the results shown. Male embryos, which are often more likely to have a 'full blown' disease because they do not have the masking X-chromosome are being discarded completely if having such a disease is a possibility. Hope this had been enlightening and interesting! Here's a link if you want the whole article---> http://www.guardian.co.uk/news/2006/jun/19/topstories3.genetics

See ya soon,
Siren.