PCR! What can we do without you?!

The Polymerase Chain Reaction or PCR for short is a process which amplifies the gene of interest in vitro. This process was not possible in earlier times as there was no known enzyme that could survive the high temperature that is required in PCR, however it all changed when two scientists named Thomas D. Brock and Hudson Freeze discovered the enzyme Taq Polymerase in an achaea which they named Thermus Aquaticus. It was able to withstand high temperatures without denaturing as it is found thermal habitats around the world and more information regarding thermus aquaticus can be found here (http://www.absoluteastronomy.com/topics/Thermus_aquaticus). There are three steps involved in PCR which is exponential amplification, leveling off stage and plateau. The product is doubled for every cycle during the exponential amplification stage and only minimum amount of DNA (gene of interest) is required. During the leveling off stage, the reaction slows down and DNA polymerase (taq polymerase) will decrease in activity. Lastly, the reaction finally stops at the plateau stage due to lack of reagents. This technique has a number of uses which include DNA fingerprinting, gene cloning and recovery of ancient DNA (http://en.wikipedia.org/wiki/Polymerase_chain_reaction#PCR_in_diagnosis_of_diseases) has more information regarding the uses of PCR.

The Brilliant Invention of DNA Microarray

Due to the advances of DNA technology, many techniques have been invented to help us to solve problems at genetic levels at a more accurate and faster manner. One of the brilliant inventions is the DNA microarray. With this method, researchers are able to test thousands of genes simultaneously to determine which ones are expressed in a particular tissue under different environmental conditions, in various disease states or at different developmental stages. For example, we can use DNA microarray to detect genes that are responsible for breast cancer. We can compare the gene expression in a healthy breast tissue and a breast cancer tissue. First, we isolate the mRNA in the healthy breast tissue and breast cancer tissue. Then, by using reverse transcriptase, red fluorescently labeled cDNA is synthesized from the mRNA from the healthy breast issue while green dye fluorescently labeled cDNA is synthesized from the breast cancer tissue. Then we put the cDNA mixture into the microarray which consists of all the human genes and allow hybridization. In the microarray, red dyes represent genes that are expressed in the healthy tissue (or more than green dyes), green dyes represent genes that are expressed in the cancer tissue (or more than red dye) while yellow are the ones that have equal amounts of red and green dyes. However, we are interested in the green dyes as these are the genes that might be responsible for causing cancer. By knowing these genes, we can develop drugs to treat those breast cancer patients. This is a breakthrough as genes that are responsible for many diseases such as AIDS can be detected by using this method and therefore can help millions of people by studying these genes.

Menopause Timing Genes Found

May 26th 2009

Scientists have found up to 20 genetic variations that bring forward the menopause for a woman, a European conference was told. The variations were found in four different places on two chromosomes, 19 and 20.The findings came from an analysis of the genes of more than 10,000 women in Britain, the USA, the Netherlands, Iceland and Italy. Researcher Lisette Stolk, from Erasmus MC, Rotterdam, Netherlands, said: "We know that ten years before menopause women are much less fertile, and five years before many are infertile.

"In Western countries, where women tend to have children later in life and closer to menopause, age at menopause can be an important factor in whether or not a particular woman is able to become a mother." A second study published last night warns that women approaching the menopause may suffer loss of learning ability.In the journal Neurology, researchers say the problem surfaces during the period just before the menopause begins - but it is only temporary. The researchers say the problem might be treated by using hormone supplements. Researcher Dr Gail Greendale said: "The good news is that the effect of perimenopause on learning seems to be temporary. Our study found that the amount of learning improved back to premenopausal levels during the postmenopausal stage."

by: 42101327
http://www.staffnurse.com/nursing-news-articles/menopause-timing-genes-found-3556.html

Study reveals startling new role for the plant hormone auxin

A team of scientists from the University of California, Davis discovered something new about the hormone auxin in plants. They found that auxin acts as a morphogen which directs the pattern of cell development based on concentration.

Plants reproduction system is located within its flower, where pollens produce sperm cells while egg cells are in the ovule. During the development stage, the ovule will undergoes both meiosis and mitosis several times. This resulting in a structure of embryo sac together with the production of 8 nuclei and three of them are positioned near the opening of the ovule. Figure below shows the position of 8 nuclei in the embryo sac.

Caption: A gradient (red) in the concentration of the plant hormone auxin, determines that only one of the eight undifferentiated nuclei in a plant's embryo sac will become an egg. (In this image, a large vacuole dominates the central section of the embryo sac.)

Credit: Monica Alandete-Saez/UC Davis

The studies discovered that the only nuclei that receive most hormone auxin will continue to develop into egg cell and later to be fertilized with sperm cell. Based on their observation, the hormone auxin is concentrated nearer to the opening of the embryo sac. Thus, the nucleus that is nearer to the opening of ovule will become egg cell. The researchers had carried out a trial to test this hypothesis where they purposely shifted the position of one nucleus nearer to end of embryo sac of plant Arabidopsis. And the result was; instead of one, two egg cells were produced.

Furthermore, they found out that this hormone auxin is produced within the embryo sac itself. This discovery may help in enhancing the fertility of crop plants where greater number of eggs could be developed into mature plants.

This article was published on June 4, 2009.
Article links: http://www.genengnews.com/news/bnitem.aspx?name=55667708
By Zaira Hidayah Mohd Arshad 42102119

'Warrior Gene' Linked To Gang Membership, Weapon Use

A new study has been carried out recently by The Florida State University that confirms an MAOA gene sometimes called the "warrior gene" link to gangs and weapons. However, this only applies to males where females seems to have resistance towards the violent effect of the gene.

'The MAOA gene affects levels of neurotransmitters such as dopamine and serotonin that are related to mood and behavior, and those variants that are related to violence are hereditary. Some previous studies have found the "warrior gene" to be more prevalent in cultures that are typified by warfare and aggression.' This MAOA gene is detected on the X - chromosome. Therefore it has more effect on males since male has one X - chromosome and a Y- chromosome while female has two X- chromosomes. For females, if there is the risk allele in one of the chromosome, there is another allele that can compensate for it. This is probably why the effect of MAOA has only been detected in males.

Link to the original article:
http://www.sciencedaily.com/releases/2009/06/090605123237.htm

by:42122809

Enzyme Necessary for DNA Synthesis Can Also Erase DNA

New mechanism that causes some changes in DNA content has been found by a group of Uppsala University scientists and it is due to something has happened in bacteria that live as a parasite inside the cells of other organisms.

Change in the amount of DNA in the chromosomes of bacteria can be either by gene amplification and gene deletion by which the amount is increasing and decreasing respectively.

Currently a genetic analysis on salmonella mutant done by a PhD student, Sanna Koskiniemi has shown that in order for spontaneous deletions are to take placed in the bacteria a special type DNA-synthesizing enzyme must be present. The decreased or increased rates of deletion up to 30 times are proven by genetically inactivating or overproducing these enzymes.
Professor Dan Andersson suggests that bacteria that live either as parasites inside cells or in symbiosis with other organisms are of special interest with regard to this new mechanism. As DNA has disappeared during evolution, thus, these bacteria often have small chromosomes. With these new findings we can better understand and predict how DNA is eliminated from chromosomes.

Link to the original article:
http://www.sciencedaily.com/releases/2009/06/090608182541.htm

By: 42111577

Cats' Central Nervous System Can Repair Itself And Restore Function

A team of researchers from the University of Wisconsin-Madison reports that the restoration in cats of myelin can lead to functional recovery from a severe neurological disorder. Myelin is a fatty substances that coats the nerve fibers known as axon and help in the conduction of nerve signals. This myelin can loss through disease causing impairment of sensation, movement, cognition and other functions, depending on which nerves are affected.

This finding is essential as myelin can be reestablished as the therapy for treating a range of severe neurological diseases associated with the loss or damage of myelin, without affecting the nerve themselves. A test also had been done to some cats to see their growth and development by giving the irradiated diet. Some of the cats show severe neurological dysfunction, including movement disorders, vision loss and paralysis. As the diet been taken off, the cats recovered slowly and all of the lost functions were restored.

article from...
http://www.sciencedaily.com/releases/2009/03/090330200722.htm

by: Nawwarah (42115799)

Blood clotting: Key Discovery

Scientists from Harvard University have discovered a molecular mechanism that is key to regulating the way blood clots.

They detected an area on the von Willebrand factor (VWF) blood-clotting protein which contains a molecular sensor to regulate the size of the protein, important for it to work effectively.
VWF is essential to the body's circulation. It controls the balance between blood clotting and bleeding. Abnormalities affecting VWF can lead to health problems such as bleeding disorders and heart attacks.

The team said that this discovery will improve understanding on how body regulates the formation of blood clots, and could also add some information into how bleeding disorders, such as von Willebrand disease, disrupt this regulation system. They also said that this finding has the potential to lead the new avenues for treatment and diagnosis.

Links to original article:
http://news.bbc.co.uk/2/hi/health/8082692.stm

More on this topic:
http://generalmedicine.suite101.com/article.cfm/blood_clotting_disorders
http://www.uch.edu/conditions/blood/blood-clotting-disorders/index.aspx
http://www.theuniversityhospital.com/adultgenetics/blood.htm
http://news.bbc.co.uk/2/hi/health/7833978.stm

Risks Of Sharing Personal Genetic Information Online Need More Study, Bioethicists Say

The advancement of the world today lead us to know our own genetic risk as easy as just provide our salive. Bioethicists from the Stanford University School of Medicine, claimed that, sharing genetic information online will raises a host of ethical questions.


As genetic information is unique in that it's not only relevant for the individuals who receive the information, but also for their family members, their children and even their children's children," said Sandra Soo-Jin Lee, PhD, senior research scholar at the school's Center for Biomedical Ethics.

"if you receive information on your breast cancer risk and share it with others, you might also be sharing information about your daughter's risk for breast cancer — even though she never consented to have that information shared."

Right now, there are nearly 100 companies around the world that provide some form of direct-to-consumer genetic testing. Customers just need to mail their DNA sample for sequencing, and then get both raw data and an interpretation of their genetic profile. After that, customers can create a public profile and share their genetic data through a company-sponsored social networking site. Due to that, experts fear that consumers may share genetic data without realizing the potential implications for themselves and their families. For now, there aren't any laws that govern the exchange of genetic information online.

article from : http://www.sciencedaily.com/releases/2009/06/090605075051.htm
picture : http://www.turbosquid.com/FullPreview/Index.cfm/ID/277513

42115696

GM MONKEY WITH JELLYFISH GENE

Eight years back ANDi, the first genetically modified monkey carried green fluorescent protein (GFP) gene which being transferred from its parents. However, this is a faulty gene since ANDi cannot glow green as expected.

Now, scientist is inserting this green fluorescent protein (GFP) gene into marmoset which is another monkey species. This is a very important research since if this genetic modification is a success, scientist will use GM monkey to study human disease since GM primates provide better model than GM mice.

For this research, viral vectors method was used to introduce green fluorescent protein (GFP) gene from jelly fish into the host cell (marmoset).The modified virus that carried the gene of interest is injected into the monkey embryos. Then, these embryos being inserted into seven surrogate mothers which four gave birth, producing 1 male and 4 female marmosets that carried the green fluorescent protein (GFP) gene.

Later, when the male baby was sexually mature, he successfully fathered a single offspring which also glowed green, showing that it had inherited the GFP gene. One of the females also produced IVF embryos carrying the gene thus shows that this research is success.

References:
http://www.newscientist.com/article/dn17194
http://www.newscientist.com/article/dn319-monkey-business.html

By:
Siti Nur Hasanah Binti Mohd Yusuf
42102052

Biofuel Production Won't Erode Global Food Supply

A newly bioprocess to produce biofuels without stressing on the global food supply has been discovered by a group of scientists in California. This approach involves the use of genetically engineered microbes with the ability to convert switchgrass, corn cobs and other organic materials into methyl halides - the raw material for producing gasoline.

Methyl halides are produced naturally by plants and microbes, but the amount is too small for commercial use. With the help of a database of 89 genes from plants, fungi and bacteria that are known to produce methyl halides, genes that were most likely to produce methyl halides were isolated and spliced into Brewer's yeast, so that these yeast cells will produce methyl halides instead of alcohol. These genetically engineered microbes boosted methyl halide production from agricultural waste to levels with commercial potential.

Prepared by:
Maisarah (42101484)

Source:
http://www.sciencedaily.com/releases/2009/05/090511115003.htm

‘Gene Silencing’ May Improved Treatment of a Deadly Complication of Liver Disease

According to Ram Mahato and his colleagues, liver fibrosis is a build-up of scar tissue in the liver. This chronic liver damage caused by hepatitis, consumption of alcohol, toxins and other factors. The liver becomes so severely damaged since advanced fibrosis can lead to cirrhosis which caused the patients to have transplant. There is no effective treatment although patients urgently need new medications. However, scientists believe that this disease emerges from protein called TGF-beta 1 which triggers liver inflammation and blocking this protein may become the treatment.



Recently, according to ScienceDaily dated June 3 2009, scientists in Tennessee have found a technique that “silences”, or turn off genes becomes a potential new treatment for liver fibrosis patients. The researches designed 10 chemically synthesized substances, siRNAs with the ability to block the TFG-beta 1 gene in the liver. Then, they tested this experiment in the rat liver cells. They found that ‘gene silencers’ decreased the level of type 1 collagen and the trigger liver inflammation to almost 50%. Thus, they suggest that gene silencing can be an effective treatment to the liver fibrosis treatment.

Resource:
http://www.sciencedaily.com/releases/2009/06/090601110517.htm

by:are-in-42101680

Scientists Identify Genetic Basis For The Black Sheep Of The Family

The typical coat color for the wild-type sheep is black with a pale belly but livestock breeders preferred uniform white coat colour domestic sheep. However,they are having problem in the sheep industry because the recessive black 'non-agouti' allele of the ASIP gene carried by white sheep is difficult to distinguish resulting in small number of black coat colour sheep in the flock. Therefore, scientists have taken initiative to determine the genetic differences at the ASIP locus in order aid the selection of white coat colour sheep.



Scientists at Commonwealth Scientific and Industrial research Organisation (CSIRO) Queensland Bioscience Precint in Australia has succeeded in identifying the allele that codes for coat colour in breed domestic sheep. The procedure involves investigation of the genetic architecture of the agouti signaling protein (ASIP) gene in several sheep breeds by sequencing the ASIP locus and measuring the gene expression. ASIP functions to regulate pigmentation in mice. It is used in this study to determine its role in expressing the coat colour in sheep.

The mechanisms of the study also involves the tandem duplication encompassing the ovine ASIP and two neighbouring genes, AHCX coding regions and ITCH promoter region. According to Dr. Belinda Norris, it was discovered that the ubiquitous expression of a second copy of ASIP coding sequence regulated by duplicated copy of the nearby ITCH promoter causes the white sheep phenotype. As for the recessive black sheep, it is expressed by a single copy ASIP gene with a silenced ASIP promoter (non-duplicated agouti alleles). The researches also studied the ASIP locus in ancient Barbary sheep and it was confirmed that, however, a single copy functional wild-type ASIP is responsible for its colour phenotype (tan body with pale belly).

It was noted by Norris, that this study will be a benchmark which aid the development of gene copy number. Besides, she stated that analysis methods in the mapping and association of heritable traits in livestock animals will be at ease as well as identifying the carrier of the black non-agouti allele. Moreover, occurence of dominant Agouti mutation also can be identified whether it occured as multiple or single events through this breakthrough.

Link to original source of article…
http://www.sciencedaily.com/releases/2008/07/080710174236.htm

By : Syikin 42101792

Hereditary Multiple Exostoses ( HME)

Definition

Hereditary multiple exostoses (HME) refers to a group of disorders characterized by abnormal bone growth.

Inherited

MHE is a condition that is passed by the genes of the affected parent to their children. It is called an ~autosomal dominant~ disorder which means that if one parent has the condition, chances are fifty percent that any child could also develop MHE. Occasionally, a patient will develop multiple exostoses with no previous family history of MHE. This situation is described as a spontaneous mutation meaning a genetic problem arose in that person without being inherited from a parent. Recently chromosomes (the packages that carry genes) 8, 11 and 19 have all been shown to be locations where the genetic information for MHE comes from. Some researchers feel there actually may be different types of MHE each caused by different genes at these locations.

Extosis

An exostosis is a bone growth that is abnormal or different from the underlying architecture of the bone. These "abnormal growths" are not cancer, They are benign. Sometimes doctors refer to exostoses as "tumors" which like exostose is a general term meaning abnormal growth. It is important to remember that not all "tumors" are cancer. Most tumors, like the exotoses of MHE, are benign. Exostoses start near the growth centers of bones which are near the ends of the bones, which is why bumps grow near the joints. They can be rounded or sharp and continue to grow while a child is growing. When a person is full grown, exostoses also stop growing.

Mutation in filaggrin gene trigger allergies

Eczema can cause the skin to become very red and itchy


Breakthrough of genetic defect in mice enable scientist to identify what factor is responsible for the rapid increase in allergic today.
Scientists in Dundee, Ireland and Japan discover the filaggrin defect in mice which causes allergic inflammation , similarly like what happen in human eczema.They found out that the filaggrin gene is very important since this gene enable skin to produce protective barrier.So, this will block the allergens from entering the body,thus preventing allergic formation.

Scientist pointed out that about one in five children in Britain and other westernised nations suffer from eczema.
Eczema cause irritating patch of sore skin,while in extreme cases ,extensive areas may become inflamed and unbearably itchy. So, the children with this condition are very susceptible to get allergic conditions, like asthma , fever and

The finding indicates that many cases of eczema are induced by genetic mutation in filaggrin gene.

The breakthrough of genetic defect of filaggrin gene enable enable scientist to develop therapies for eczema and other allergies by suppressing the defective filaggrin gene.Now, scientists are still looking for the drugs or treatments that aim at the filaggrin gene and hopefully they will find the cure for these disease in recent time.


REFERENCE…
Mouse Gene Aids Allergy Research 2009, BBC News, 6 April, viewed 28 May 2009 at


Link to original source of article…
http://news.bbc.co.uk/2/hi/uk_news/scotland/tayside_and_central/7985307.stm

42101765
TUC/UQ STUDENT

World First: Chinese Scientists Create Pluripotent Stem Cells from Pigs

A scientist named Dr Xiao and colleagues have managed to induce cells from pigs to transform into pluripotent stem cells (cells that, like embryonic stem cells, are capable of developing into any type of cell in the body). It is the first time in the world that this has been achieved using somatic cells (cells that are not sperm or egg cells) from any animal with hooves (known as ungulates).

Dr Xiao succeeded in generating induced pluripotent stem cells by using transcription factors to reprogram cells taken from a pig's ear and bone marrow. After the combination of reprogramming factors had been introduced into the cells through a virus, the cells changed and developed in the laboratory into colonies of embryonic-like stem cells. Further tests confirmed that they were, in fact, stem cells capable of differentiating into the cell types that make up the three layers in an embryo – endoderm, mesoderm and ectoderm – a quality that all embryonic stem cells have. The information gained from successfully inducing pluripotent stem cells means that it will be much easier for researchers to go on to develop embryonic stem cells that originate from pig or other ungulate embryos. Dr Lei Xiao, who led the research, said: “it is entirely new, very important and has a number of applications for both human and animal health."

Pig pluripotent stem cells would be useful in a number of ways, such as precisely engineering transgenic animals for organ transplantation therapies. They could also be used to create models for human genetic diseases. However, Dr Xiao warned that it could take several years before some of the potential medical applications of his research could be used in the clinic.


Reference: http://www.sciencedaily.com/releases/2009/06/090602192557.htm


By: s41461846

Possible cause of Alzheimer’s disease caused by hyperphosphorylation of tau proteins may have a genetic link.

A recent discovery by researchers at McGill University and Lady Davis Research Institute for Medical Research at Montreal's Jewish General Hospital promises to help in the diagnosis and curing of Alzheimer’s disease. They found that in patients will AD, there was a hyperphosphorylation (extra phosphate added) to one of the amino acids on a tau protein in the CNS. The 6 isoforms of Tau proteins are involved in the stabilisation of microtubules by their reaction with tubulin. When they are hyperphosphorylated, it causes a protein cascade with interaction between tau proteins resulting in neurofibrillary tangles that cause the neuron transport system to fail. This causes incorrect signals to be sent, and eventually neuron death. These tangles often occur in older individuals, but not on nearly as large a scale as in a patient with AD. A protein called beta-amyloid that builds up in neurons is also associated with AD, and thought to help cause cell death by interrupting cell homeostasis, causing apoptosis. By investigating the cause of this hyperphosphorylation, and build up of beta-amyloids, researchers hope to eventually find a cure for AD, as they believe that this hyperphosphorylation may be genetically linked. APOE is a gene that is present in 50% of late-onset Alzheimer’s disease cases. Genetic interpretation of this gene could help to find a cure, and genetic modification of this gene in embryos could also help to cure it.

This discovery is very important, as Alzheimer’s disease is a very prominent disease in society’s elderly, and can have disastrous effects, such as initially short-term memory loss, then as the disease progresses, resulting in greater cognitive degeneration, confusion, irritability, mood swings, language breakdown and long-term memory loss. This draws on many of the concepts covered in the course, such as protein interactions, protein cascades, genetic modification and interpretation.

http://www.ncbi.nlm.nih.gov/pubmed/11801334

http://www.genengnews.com/genCasts.aspx

Andrew Buchan - s4202068

Genetics Can Mediate Vulnerability To Alcohol’s Effects During Pregnancy

Teratogenesis is a condition that affects embryos causing defects in their development. A likely cause of teratogenesis is the consumption of alcohol while pregnant. This condition results in Foetal Alcohol Spectrum Disorders (FASD), which refers to a wide-array of effects due to alcohol-exposure. It occurs in approximately one percent of live births in the United States. However not every woman who consumes alcohol while pregnant gives birth to children that have observable deficits.

A study done on mice has presented that alcohol-related susceptibility and resistance may be attributed to genetics.

To do the study, the researchers, led by Chris Downing, a research associate at the University of Colorado, used mice so they could control a variety of variables that impact teratogenesis and FASD. To control the differences in genetics the researchers bred five inbred strains of mice. They did this because every individual in an inbred strain is “virtually genetically identical, greater than 99.9 percent”.

The researchers gave the pregnant mice 5.8g/kg of alcohol (or malto-dextrin) on the ninth day of pregnancy which is approximately equivalent to day’s 28-31 of the human gestation period. On the eighteenth day of pregnancy the mice were put down and the foetuses were examined to identify any ‘gross morphological malfunctions’.

It was revealed that one strain of mice had foetal weight deficits. This strain also had malformations of the digits, kidney, brain, ventricle and vertebrae. Another strain, however, showed no obvious evidence of teratogenesis. The three remaining strains all showed varying degrees of teratogenesis.

These results emphasise that genetics does play a role in teratogenesis as the different genetic strains of mice are affected in different ways.

There is the possibility that these results could be extrapolated to human teratogenesis as mice and humans have an astonishingly similar genome, so it is reasonable to suggest that genetics could play a role in human teratogenesis as well.

Article Link:

http://www.sciencedaily.com/releases/2009/04/090422175142.htm

By Lachlan Hooper (42065607)

Stem cells without defects

It may now be possible to create stem cells from a patients own body which contain their own DNA except for the the target mutation. Scientists have recently reprogrammed tissue cells, from patients with anaemia, into stem cells which include the patients DNA sans the mutations responsible for their condition. These resulting cells are then grown into blood precursor cells which are the type that are usually transplanted into patients with this type of anaemia. In this case however, they contain the patients DNA rather than the donors.

Even though this hasn't been trialled on humans yet, it is a an important proof of concept, as well as being a significant breakthrough in the treatment of patients with genetic conditions.
Since these cells contain the patients own DNA, they can be introduced into their body without the risk of them being rejected by the body's immune system. In other words, the cells were identical to the patients original cells except that they didn't contain the genetic mutation responsible for the disease. Even though there still need to be a few more modifications to this process, it is a proof of concept, as well as being a significant breakthrough in the treatment of patients with genetic conditions.

42023915
Original article:http://www.timesonline.co.uk/tol/news/uk/science/article6402006.ece
Image:http://www.usask.ca/alumni/alumnisite/publications/green_white/issues/spring2006/cover_story.php

Huntington's Disease and Depression: The missing link

Huntington’s Disease (HD) is a dominantly inherited genetic neurodegenerative disease. The disease is due to a mutation in a single causal gene, the Huntingtin gene, which results in an abnormal form of the protein Huntingtin. This mutation ultimately leads to the degeneration of motor neurons in the brain resulting in uncontrolled movements, loss of mental capacity and emotional disturbances.

One emotional disturbance, which has been closely associated with those affected by HD, is clinical depression. It has long been thought the depression associated with this is due to the fact genetic tests now allow for testing at any age, typically before onset of any symptoms, and the social reaction of knowing you have the disease. The dominant nature of the disease means enormous stress is often put on those finding out they carry the gene not only because it is known they will be affected by the disease later in life, but also because carrying the disease means having a 50% chance of passing it onto any offspring. The pedigree to the left shows the dominant nature of the heritability of Huntington's Disease.

Until recently this abundance of clinical depression was thought just to be due to the knowledge of knowing one had a life-threatening disease. Research by the University of British Columbia has sought more actively for the causes of these emotional disturbances. Scientists found that mice with a defective Huntingtin gene showed signs of depression when the protein was altered. After repairing the Huntingtin protein the mice showed no more symptoms. Additionally the study explored the effectiveness of the two most common drugs, tricyclic and SSRI antidepressants, used to treat depression in people with HD and found they were ineffective at treating the depression in mice caused by the mutant Huntingtin gene. This study was based upon work by Dr. Hayden who in 2006 was able to prevent the cleavage of the Huntingtin protein in mice and as a result cure the degenerative symptoms in those mice. This study has shown much potential into one day finding a cure for the devastating HD.

Posted by Simon Yates, 41789072, Thursday P10

Reference:
http://www.physorg.com/news159200198.html

Link between MS, vitamin D and sunlight gives some bright hope.

Multiple Sclerosis (MS) is a degenerative disease of the central nervous system which is characterised by ‘myelin loss, axonal pathology and progressive neurological dysfunction’ [1]. While there is no known cause for MS, both genetic and environmental aspects are recognised as having significant impact. The strongest impact on the genetic risk of acquiring MS is linked to an allelic variation within the Major Histocompatibility Complex (MHC ) Class II Region. Within the MHC, a region at or near the HLA-DRB1 locus impacts on the risk of MS with ‘the dominant haplotype (group of alleles or genes) of Northern Europe, marked by the presence of DRB1*1501, [increasing] the risk of Multiple Sclerosis by 3-fold’ [1].

Research has also revealed a significant correlation between geographic location and prevalence of MS which, in the Northern Hemisphere, shows a ‘north-south gradient, mirrored by a south-north gradient in the Southern Hemisphere’ [1]. This geographic distribution of the disease suggests that sunlight, through its role in producing vitamin D, is a key environmental factor associated with the risk of MS. Previous evidence of the roles that vitamin D has on the development and function of the immune and central nervous systems suggest how a lack of vitamin D could affect the risk of MS, yet no direct link had been established. This research discovered that vitamin D was directly related to the expression of the HLA-DRB1*1501 gene.

In conclusion, this study provides evidence to support previous beliefs that: sunlight and vitamin D are intrinsically related to the risk of MS, implying that the supplementation of vitamin D to individuals at specific times may be vital in the prevention of MS. Hence, this study has implications on research into the prevention of and efforts to find a cure for this disease.

Reference [1] :

Ramagopalan SV, Maugeri NJ, Handunnetthi L, Lincoln MR, Orton S-M, et al. (2009) Expression of the Multiple Sclerosis-Associated MHC Class II Allele HLA-DRB1*1501 Is Regulated by Vitamin D. PLoS Genet 5(2): e1000369. doi:10.1371/journal.pgen.1000369

Source of the picture:

http://www.msaustralia.org.au/msra/news-media/news.ph

Link to Original Source of the Article:

http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1000369

Posted by: Erica Ortt

Student #: 4202 6466

Saved By Junk DNA

Researchers have found that DNA which was previously though to be ‘junk’, could play a vital role in the evolution of the genome.

It seems that tandem repeats influence the activity of neighbouring genes. How tightly local DNA wraps around nucleosomes is determined by these repeats. This packaging structure then dictates the extent to which genes can be activated. As these tandem repeats are very unstable the number present changes frequently during DNA replication. This changes the way DNA is packaged and activated.

These changes may allow organisms to tune the activity of their genes to match the environment. This is a vital principle for survival.

To test this idea scientists conducted a complex experiment testing tandem repeats in evolution using yeast cells as guinea pigs. It was found that when repeats were present near a gene it was “possible to select yeast mutants that show vastly increased activity of this gene”. When the tandem repeats were removed however this evolution was impossible.
As the researchers said “If this was the real world only cells with the repeats would be able to swiftly adapt to changes, thereby beating their repeat-less counterparts in the game of evolution. Their junk DNA saved their lives”.

Posted by 42053707
Link: http://www.medicalnewstoday.com/articles/151864.php

Memories may be stored in DNA

Recent experimentation in mice leads to suggestion that patterns of chemical ‘caps’ on deoxyribonucleic acid (DNA) may be responsible for preserving memory.

The recollection of a particular event requires a specific succession of neurons to trigger just at the right time. For this to occur, these neurons must be connected in a particular sequence by chemical junctions, referred to as synapses. It remains a mystery how these synapses endure over decades, given the proteins in the brain, including those that form synapses, are destroyed and replaced constantly.

Courtney Miller and David Sweatt of the University of Alabama (Birmingham), suggest that long-term memories may be preserved by a process termed DNA methylation - the addition of chemical ‘caps’ in the form of methyl groups onto our DNA. There are methyl group substituents already present in many of the genes within our genome. At the division of a cell, this alleged “cellular memory” is passed on and tells the new cell what type it is - for example, a kidney cell. Miller and Sweatt argue that in neurons, methyl groups also assist the control of exacting patterns in protein expression required to maintain the synapses that constitute memories.

They started by looking at short-term memories. When caged mice were given a small electric shock, they normally freeze in fear when returned to the cage. However, injecting the mice with either of Hydralazine hydrochloride (1-hydrazinophthalazine monohydrochloride) or Procainamide (4-amino-N-(2-diethylaminoethyl) benzamide to inhibit methylation seemed to erase any memory of the shock. The researchers also showed that in untreated subjects, gene methylation changed rapidly in the hippocampus region of the brain for an hour following the procedure. A day later, it had returned to normal, suggesting that methylation was involved in creating short-term memories in the hippocampus (Neuron, DOI: 10.1016/j.neuron.2007.02.022).

To determine whether methylation is elemental in formation of long-term memories, Miller and Sweatt repeated the experiment, this time observing reaction in the cerebral cortex (centre for memory, perceptual awareness & consciousness). It was found that methyl groups were being removed from a gene called calcineurin and allocated to another gene. As the exacting pattern of methylation eventually stabilised and remained constant, the researchers determined that the methyl alterations may be anchoring memory of the shock into long-term memory, rather than just controlling a process involved in memory formation.

The findings of this experiment were that short-term memories forming in the hippocampus slowly turned into long-term memory in the cerebral cortex. “The cool idea here is that the brain could be borrowing a form of cellular memory from developmental biology to use for what we think of as memory”.

References
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Tomkoya, J, Friedecky, D, Polynkova, A, Adam, T 2009, ‘Capillary electrophoresis determination of thiopurine methyl transferase activity in erythrocytes’, Analytic, Technological & Biomedical Life Science’, viewed 24 May 2009.

42021117

Bacteria Could Prevent Mosquito Propagation of Dengue Fever

Dengue Fever is a rapidly spreading mosquito born disease whose symptoms range from mild aches and fatigue to severe joint and muscle pain. However the most sever form of the fever has a fatality rate of 1 in 20 and eventuates when multiple strains of the virus are present. There is currently no cure for the disease and there are fears that the disease could become an endemic. The ailment is carried in particular by a mosquito bread that feeds almost exclusively on human blood called Aedes aegypti. Once the mosquito bites an infected person the virus is transferred to it and begins replicating. The virus can then be passed on to other humans through biting.

One way of preventing the spread of Dengue Fever is by modifying the mosquitoes so that they die before they can pass on the disease as the incubation period of the virus is relatively long. This can be done through infectious bacteria known as Wolbachia which are transferred through the host’s eggs. Consequently the bacteria have become adapt in maximising the number of infected eggs, causing selection for infected offspring through genetic mutations of the host. This is seen as the infection spreads rapidly through the population. Therefore if a strain of Wolbachia which shortens the bacteria’s lifespan it can stop the propagation of dengue as the mosquito will die before the incubation period is complete. However the strain of Wolbachia that reduces an insect’s life span usually infects fruit flies and thus a new strain needed to be synthesised. This was achieved through the application of genetics as the Wolbachia bacteria was injected into A. aegypti and the bacteria that were able to evolve and survive in the mosquito were selected. The end result is that the Wolbachia can now affect mosquitoes, shortening lifespan in a treatment method that could extend beyond simply preventing the propagation of Dengue Fever but other insect born diseases as well.

Posted by Zahed Lambat, s4205101, Tuesday P3

Link: http://www.newscientist.com/article/mg20227101.400-genderbending-bugs-could-tackle-mosquito-plagues.html?full=true