Obesity - Caused by genes from our past?

As most of you will know, obesity is a serious problem in developed countries such as Australia and the US, and is becoming more and more prevalent with each passing year. The major reason for this predisposition to obesity is the culture in which we live, a culture that promotes fast food and higher calorie intake in conjunction with minimal physical activity. According to the Medical Research Council Epidemiology Unit, Institute of Metabolic Science, Cambridge, UK, genes that might have provided a method or survival under circumstances of famine in the past, may be causing a predisposition to obesity in a culture where food is abundant. Two studies were conducted, one being genome-wide linkage studies where the whole genome is examined to identify the approximate location of new genes for a disease or trait of interest, the other being candidate gene studies, an approach that relies on current understanding of the biology and pathophysiology of obesity and related traits. Genome wide studies have led to a dramatic increase in the amount of discoveries of genetic loci which give cause to various diseases or traits, however the rate of discovery of obesity linked loci is much slower, since obesity is a multifactorial characteristic that extends from environment, exercise etc. The studies resulted in a discovery gene FTO, which seemed to be in close correlation with cases of obesity and body mass index. Although this gene was the only conclusive result gained, there is no doubt that there are many more un-detected obesity-susceptible loci hidden amongst false positive test results and the limited power that a single genome association study provides.

By 42015826

Source: http://ovidsp.tx.ovid.com.ezproxy.library.uq.edu.au/spa/ovidweb.cgi?QS2=434f4e1a73d37e8c776ba62893c7002df7fec0bb114a0d35b63f7257ce5cc91b47dd50c4c70d1b57a74803bebedf0933758c4952f0f8f243571e4bb9cffc31a3f8401bdfc35ee6be79a19486d39703feea829e436d54fec454b83346f0be52a3bff2386309380372a7c3ed31183e592fdc4a808f05fe1c134ba2706ca81eb99a3fc524d288eba2626c37c5bff04bdfbd87971ad9b5e00668246effe1a5f8b898f74b925e74fe0f52342690e074b5072789b2cbd6351610e2c39b08a0f28dbf8224f60e51bad5e3abf9615bd1ce18d3e3876393c633282e682c57f80bae9e1365277c579c963775cdceb6a773551cc9e4

MAOA - If You Have This Gene, You're More Likely To Join A Gang?

Boys who carry a particular variation of the gene Monoamine oxidase A (MAOA) often called as warrior gene are more likely to join gangs and be among their most violent members, according to a study from a Florida State University.

Monoamine oxidase A gene affects levels of neurotransmitters in the brain such as dopamine and serotonin that are related to mood and behaviour, and those variants that are related to violence are hereditary.

This effect of the gene applies only to males because of its location on the X-chromosome. Males, who have one each of X-chromosome and Y-chromosome, possess only one copy of this warrior gene, while females carry two having two X-chromosomes. Thus, if a male has an allele (variant) for the MAOA gene that is linked to violence, there isn’t another copy to counteract it. However, females have two copies, so even if they have one risk allele, they have another that could compensate for it. This is why the MAOA effect has only been detected in males.

Participants were drawn from the National Longitudinal Study of Adolescent Health of 1155 females and 1041 males, and the low MAOA activity alleles conferred an increased risk of joining a gang and using a weapon in a fight for males but not for females. Moreover, among male gang members, those who used weapons in a fight were more likely to have a low MAOA activity allele when compared with male gang members who do not use weapons in a fight.

http://www.comppsychjournal.com/article/S0010-440X%2809%2900049-2/abstract
41612237 Soo yeon Yoo

Sleep Genes Identified

Sleep is a behaviour that is common in all animals but the reason to how lack of sleep can affect the animal’s condition requires further investigation. A study was done to look more closely at this behaviour from sleep and activity patterns of 40 different lines of wild Drosophila melanogaster (fruit flies) at the genetic level as it may contribute to the understanding of human sleep. The fruit flies were homozygous but the lines were different and each one of these flies were placed in a small glass tube which were connected to a machine that monitored the activity of the flies every minute using infrared sensors. The study found that in male flies, the duration of sleep was longer than female flies on average. Also, males slept more during the day and were more active when awake than females. Almost 1700 genes were identified in the study and some were not known to have an effect on the variability of sleep in fruit flies before this study was conducted. Some genes that were thought to have an effect on sleep duration were verified by separate mutations in those important genes and effects on sleep duration were observed. Groups of genes that affect sleep were identified in the study and now there is a greater understanding of how genes relate to sleep.

By 42066350
http://www.sciencedaily.com/releases/2009/02/090222142149.htm

Genetics: The Key to Domestication

Have you ever wanted to own a pet tiger, but thought it was impossible for safety reasons? This may become a reality in the future. Scientists in Germany are investigating the genetic changes underlying the differences in behaviour, which may lead to the domestication of wild animals.
In one experiment, tameness and aggression were compared in rats, as scientists believe this is the underlying principal in domestication. To determine if behaviour differences are due to gene differences, as opposed to the environment, the pups of aggressive rats were swapped with the pups of the tame parents; the pups were to be reared by behaviourally different parents. Consistent to expectations, the fostered rats showed behavioural characteristics of their genetic parents, thus demonstrating that behaviour differences are genetic. Simply investigating and comparing the DNA of the tame and aggressive rats, would not allow gene variants to be concluded, so the rats were cross-bred. In the second generation, the hybrids had behavioural characteristics ranging from exceedingly tame to immensely aggressive, and these were matched against genetic markers. The results highlighted key regions of the genome (at least five genes with complex interactions) which were responsible for tameness. Research is currently being conducted to pinpoint the mutations and the genes responsible for the behavioural differences.
In the future, these findings will be compared to research conducted on silver foxes, which found that tame foxes have a ‘reduced activity of the hypothalamic-pituitary-adrenal axis’ (controls response to stress) and had higher levels of serotonin (neurotransmitter responsible for inhibiting aggressive behaviour). If a common genetic link is discovered between the different organisms, research will be conducted to find similar genes in other organisms in the hope that wild animals can be safely domesticated. If successful, comparisons will be made to the human genome to further understand human behavioural differences. Scientists hope that pharmaceutical companies will exploit the findings to successfully treat behavioural disorders in humans.
By 42027614
For more information visit:
My Little Zebra: The Secrets of Domestication
http://www.newscientist.com/article/mg20427281.500-my-little-zebra-the-secrets-of-domestication.html

Susceptible to Melanoma?

Excessive sunlight exposure is commonly associated with skin cancer. At the present moment, Australia is ranked number one in having the highest incidence of skin cancer in the world. A whopping figure of more than 10,000 cases are being reported each year.

Recently, research conducted on melanoma, the deadliest form of skin cancer, has shown that excessive sunlight exposure is not the only contributing factor to the disease. Researchers believe that there may be another important factor that could allow them to pinpoint a person’s susceptibility to melanoma. It is GENES. They have discovered two gene variants that play a role in increasing a person’s risk of getting melanoma, and these gene variants act by increasing the number of moles on a person’s body. Though the chances of a person carrying even one gene variant is very slim, research has shown that should a person carry just one of the two genes, this will increase his/her risk in developing melanoma by 25%. A person who carries both gene variants, will increase his/her risk to about 50%. At present, these findings are still very new, and will require a lot more research. As researchers now have a more in-depth understanding of the relationship between melanoma development and mole formation, this knowledge gained is hopefully the beginning of many more new discoveries.

Though the two newly discovered gene variants will enable researchers to develop some form of diagnostic or screen tests, they hope that in the next 2 to 3 years, they would be able to collect a pool of 10-20 different gene variants. With this, researchers will be able to look at them simultaneously to calculate a person’s risk to melanoma.

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http://www.abc.net.au/news/stories/2009/07/06/2617446.htm

Proteins and Male Infertility, the streamlined sperm

The sperm cell is the only cell that swims and the speed of the sperm is critical in fertility. Just like how swimmers can wear suits to increase their speed, the male sperm has developed their own way to become specially streamlined. A study by scientists at the European Molecular Biology Laboratory (EMBL) show that there is a protein found in the developing sperm called Brdt that causes re-packaging of sperm DNA by utilizing the proteins called histones.
We know that in our body our DNA is packaged into structures called chromatin. The long DNA strands our wrapped around the proteins, histones, in what is known as the histone complex. It is found that in sperm, this complex is much more compact making the size of the head small for greater streamline effect. The compactness of chromatin is regulated by histones which are marked with different chemical tags. These tags can bind to different proteins that act as a code for structural change. The protein Brdt binds strongly to two tags in the histone complex as opposed to the norm of one tag. Therefore Brdt is able to cause greater compaction by pulling the histone complexes together once the histones have been tagged. Upon examining other proteins that deal with chromatin, this tag-binding process is most likely to be used as well, increasing our understanding of the histone code. Further research in on this in sperm development may show greater understanding of the protein and its role in human infertility.

For further reading visit:
http://www.sciencedaily.com/releases/2009/09/090930132652.htm
By: 42043007

Gene linked found for better treatment of Type 2 diabetes

Type 2 diabetes is characterized by high blood glucose due to insulin resistance and relative insulin deficiency. The discovery by diabetes UK on variation in gene CYP2C9 may provide better effective treatment for the disease. The person with the variant in the gene s is three times more likely to have good glucose level in the blood when taking with diabetes drug. The study is done by looking at 1,073 people with Type 2 diabetes who had been treated with sulphonylureas . The results show that six people in every 100 people with two variants of the gene CYP2C9 were 3.4 times more likely to achieve good glucose level range. The variation in the gene can reduce the effectiveness of the gene to produce enzyme that can break down sulphonylureas in the liver. Hence the treatment can be tailored for person according to their genetic makeup. This will reduce the cost that is used for ineffective drug treatment. All in all, this new discovery can lead to effective treatment for type 2 diabetes.

Source: http://www.medicalnewstoday.com/articles/166669.php

41936719

DOG BREEDING

DOG BREEDING - 42054692

A controversial British documentary about the breeding of dogs has stunned the Australian public. Nowadays, one of the main criteria of dog breeding is “appearance”. Experts claim that the general public are ill-informed of the health issues involved with cross-breeding, and thus, have placed an unjustified emphasis on the appearances of dogs rather than their well-being. Currently in Australia, there are thirty-five most popular dog breeds. Among these well-liked breeds is at least one inherited genetic disorder which is associated with breeding standards.



Image: Dachshund from the present day and a painting of a dachshund from 1906 - Notice that the difference in the length of the leg and the neck.

Dogs with congenital problems due to interbreeding often suffer epileptic fits or ‘spasms’. In some cases, some breeding dogs are born partly paralysed because their brain is much too big for the skull. This breeding article argues that some dogs are better to be purely bred because their distinctive physiological features can be retained. Also, in case of dog breeding, the gene analysis is needed beforehand.

http://www.abc.net.au/news/stories/2009/09/11/2682934.htm

Bar Flies: Fruit Flies Help Unravel the Genetics of Alcohol Sensitivity

After effectively using fruit flies, scientifically known as Drosophila melanogaster, for various genetic related endeavours, a group of scientists at the North Carolina State University has recently used this species to investigate the genes which contributes to alcohol sensitivity. Fruit flies are able to be used as a model for finding the genes involved in human alcohol sensitivity because flies are also susceptible to becoming drunk. Similar to humans, “drunken” flies have problems with their movements and show signs of sleepiness.

To identify the genes related to alcohol sensitivity, over 25 generations of fruit flies were bred. There were two distinct groups within this population: flies that were highly sensitive to alcohol and those that were highly tolerant of alcohol. The entire genomes of the flies (in the two groups after 25 generations) were then expressed and analyzed for comparison with the genomes of the flies in the very first generation/original population. The expressed genomes of the two groups of flies (highly sensitive and highly tolerant) were also compared with one another. These comparisons allowed the researchers to identify the differentially expressed genes between the two groups. These genes are the ones that scientists suggest are linked to alcohol sensitivity.

This experiment identified over 1000 genes that were expressed differently. By knowing these genes, scientists can compare with or look for similar genes in the human genome. This knowledge can be used to possibly help alcoholics or prevent those with high alcohol sensitivity from becoming alcoholics.

http://www.sciencedaily.com/releases/2007/10/071030184518.htm

42027007

Eat but not get fat!

The problem of obesity is alarming, especially in Australia. Females in their teen years often go on diet to appear slim and attractive. The worry of getting fat from eating too much is everywhere. Pretty sure majority of people wish that one day, we are able to eat without having to worry what we ingested are going to do to our looks. Having this dream, is it possible that one day, humans are able to eat but not get fat?

UK researchers have successfully found the gene that is responsible for turning carbohydrates into fat. This gene is known as DNA-PK, and is known to regulate the process of turning carbohydrates into fat in the liver. Experiment with mice has been conducted and shown that DNA-PK deficient mice stayed slim even when fed with the same amount of food as the control group. Results showed that the DNA-PK disabled mice had 40% less fat than the control group. Moreover, the scientists also discovered that the mice with DNA-PK gene removed had lower level of blood cholesterol as well. Lowered blood cholesterol means that the risk of heart disease is reduced as well.

Since both mice and humans have the same gene, scientists believe that this gene discovery has provided new clues to how the body metabolises carbohydrates and their contribution to obesity. Also, this gene discovery might provide a new solution to obesity and heart disease.

Available online at: http://www.abc.net.au/news/stories/2009/03/20/2521588.htm

The Sweetness of Nectar

People commonly give loved ones flowers as gifts whilst they rarely consider how these plants can be so beautiful. Floral nectar is fundamental in the life cycle of both plants and animals which pollinate them. Plants provide nectar to animals, such as bees; in return, the animals transport the pollen to surrounding plants. Nectar consists of a sugar-rich fluid which is composed largely of glucose, fructose and sucrose. There are several disadvantages to the plant which produces this nectar. Some of these issues include the fact that, nectar is quite costly to produce, the sweet sugar produced attracts pathogens as well as pollinators and even if it does successfully get transported by the pollinators, the pollen may not reach the correct plant species for fertilisation to occur. These issues are a reflection of the high complexity in studying the mutual relationship between flowering plants and the animals which pollinate them.

Through the past, scientists have attempted to study the genetics behind nectar without much success. However, recently, there has been a breakthrough. People have developed new technologies which enable scientists to design plants which have genetically modified nectar. These designer plants are then grown in controlled environments and the genetic changes can be observed through these controlled interspecific crosses. The P.intergrifolia produced significantly lower amounts of nectar in controlled laboratory conditions than in the P. axillaris sister species. Such occurrences opens up new opportunities for scientists to study the genetic changes which took place to result in different nectar and plant physiology. Further advances in this field of genetics will definitely answer many questions about the mutual relationship between plants and their pollinators.

http://www.sciencedirect.com.ezproxy.library.uq.edu.au/science?_ob=ArticleURL&_udi=B6VS4-4W9Y3DV-1&_user=331728&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000016898&_version=1&_urlVersion=0&_userid=331728&md5=9034ad8694e4e44252032413b89aa130

Gaining Insight into DNA transposition

It was not long ago since the DNA trasposition had been shown to play vital roles in the development of an organism. Transposons, or the 'jumping genes' which were once thought of as junk DNA are now believed to have significant effects on the behavior of neighbouring genes as the realignment of antibody genes in human genome has been shown to enable the immune system to fight infection more effectively.

Based on that, researchers from the University of Edinburgh discovered the roles of protein in the DNA transposition as to how enzyme can cut out sections of DNA to be reinserted elsewhere in the genome. Studies showed that DNA transposition which involves a cut and paste mechanism are mediated by transposon-encoded transposase proteins that catalyze transposition through an specific order of events. Firstly, the transposase will bind specifically to the terminal inverted repeats (IR) present at each end of the transposon forming a paired-end complex (PEC). After that, cleavage of DNA strands would be formed at each transposon end to release the target DNA. The DNA strand released will then be transfered to a new site.

The discovery of the exact mechanism of DNA transposition mediated by the transposase enzyme has implied further possibility of manipulating human genome. As suggested by Dr. Julia Richardson who led the study, this research has given us a clearer picture as to how protein should be adapted and controlled which enable genes to be inserted into cells exactly where they are needed - the ultimate aim of gene therapy.


Further reading: http://www.impactlab.com/2009/09/24/junk-dna-cut-and-paste-protein-discovery-may-prove-invaluable-in-quest-for-gene-therapies/


Kuan Chuan TAN 41936166

Human Epigenome : The Mould For Humanity

From a paper published on the 14th October issue of Nature, scientists has successfully uncovered the first complete high resolution map of human epigenome. The epigenome is described as being the template from which gene expressions are regulated. This means that epigenomes actually decide how a person grows and develops under influences from our daily lifestyles and environment. In another way, epigenome is thought as the factor that what phenotype is expressed from all the possibilities of the complete genome.

The scientists behind this work, Dr Joseph Ecker and colleagues, told the media that this research will greatly help the advancement of treatment for various diseases. However, the effects of medications which interact with the epigenome has to be fully understood in the future before these drugs can be used freely.

For this study, human embryonic stem cells and fibroblasts were compared and from their epigenomes, Ecker and colleagues found that there is a group of methyls which is the functioning pathway of the epigenome.

There are two ways for the epigenome to act on the genome. One way is to target the histone which restricts access to DNA while the other, which is the focus of this new research is the methylation of DNA. Cytosines are commonly followed by guanines in fibroblast cells as previously expected(known as CG methylation), however in embryonic stem cells this pattern was not always how things worked out. Later, the team sought to prove this by using another stem cell line and fibroblast cells and they discovered that indeed there was a high level of non-CG methylation until when they differentiate.

The team believes that their work will be very highly valuable for improving our understanding of genes and grealty help us advance in treatment of cancers and mental illness.

41936885 Sang Geng ONG

"Human DNA methylomes at base resolution show widespread epigenomic differences."
Ryan Lister, Mattia Pelizzola, Robert H. Dowen, R. David Hawkins, Gary Hon, Julian Tonti-Filippini, Joseph R. Nery, Leonard Lee, Zhen Ye, Que-Minh Ngo, Lee Edsall, Jessica Antosiewicz-Bourget, Ron Stewart, Victor Ruotti, A. Harvey Millar, James A. Thomson, Bing Ren & Joseph R. Ecker.
Nature Published online 14 October 2009.
DOI:10.1038/nature08514
link to article : http://www.medicalnewstoday.com/articles/167591.php

Stress CAN reverse the aging process!

Every organism has to deal with exposure to stresses and this applies to cells as well. Despite the popular belief that stress can cause cell death and hasten the aging process, a research conducted by biologist Sandy Westerheide and her group from Northwestern University found results that suggest otherwise. In actuality, stress can prolong life, provided that the stress is mild and sub-lethal. The research discovered a new regulated mechanism that cells use to prevent protein damage from stress.

The study focused on an enzyme Sirtuin 1 (SIRT1), a protein that is activated by the chemical resveratrol, which is found in red wine. Already known for its link to aging, the role of SIRT1 is to deacetylate proteins, which contribute to cellular regulation, allowing it to stay on the DNA and to keep producing special protein repair molecules (which work to prevent cell death and extent the life of the cell). Controversially, newfound evidence was discovered by the scientists who suggested that SIRT1 also regulated heat shock response (the damage-limiting of cells and organisms to protect against other stresses) in human cell lines. Variables of mild stress were experimented and results showed that when under mild stress, heat-shock response increased, as well as the level of SIRT1. Westerheide explained that this mechanism was due to the removal of the acetyl groups which allowed more protein repair molecules to be produced. The researchers concluded that the cell is protected against damage when more of SIRT1 is activated under mild stress conditions.

Although the study only tested on human cell lines, the scientists hope that with a greater understanding and further discovery of the heat shock factor 1, SIRT 1 and of the two functioning together they may be able to introduce a mechanism that may be able to protect the cells of whole organism as well. If this is successful, we may be able to alter and manipulate lifespan.

Read more at:

http://esciencenews.com/articles/2009/02/19/anti.aging.pathway.enhances.cell.stress.response

http://www.sciencenews.org/view/generic/id/41044/title/Antiaging__A_little_stress_may_keep_cells_youthful

Second Genetic Link To Obesity Identified

Obesity is simply the body mass index that is greater than 30Kg/meter square with more than 30% of Americans being obese and obesity also constitutes 5-7% of National Health spending (Walley, Blakemore & Froguel, 2006).The number of obese children has also tripled in the last thirty years. A new genetic variation that affects individual’s fat mass, abosolute weight and disposition to obesity was recently found. A mutation in MC4R gene usually results in familiar obesity which makes children of obese more at risk than other children whose parents are not obese (MRC, 2008). The study established that individuals possessing copies of MC4R genetic variant gain an average weight of 1.5 kg compared to those who do not have the variation. Similarly, the FTO gene has also been held culprit and individuals who carry two copies of the FTO variant also have higher weight of about 2-3 kg on the average compared to persons with no copies of the variation (MRC, 2008).
Individuals who have both the FTO variant and the recently discovered MC4R together were 3.8kg heavier on average. The third identified gene in causation of obesity is the NeXN3 (Neurexin gene 3), the same gene that has been linked to addiction and alcohol dependence as well as substance abuse. Identifying genes responsible for obesity may help to produce drugs that can target the molecular pathways via which obesity genes carry out their effect (Scientist Live).
The fourth gene that has also been implicated in a study, in the causation of obesity is the ENPPI gene which contributes to obesity in children and also simultaneously increases diabetes risk. The study revealed that obesity is majorly inherited from grandparents and parents to the children. The conclusion was reached when researchers found similar patterns in the risk of obesity in children parent and grandparent. (Biomedicine, 2008).
Fat cell biology reveals that obese children have more fat cells and this is regarded as hyperplasic obesity which is also genetically determined..Genetics influences close to 70% of obesity. Sixty percent of children with single parent obese come down with obesity while the percentage increases to eighty percent when both parents are obese. Finally, a protein called leptin is produced by the OB gene (obese gene) and this leptin circulates in the human blood (Q&A, 2009) The lepton also acts on the brain and signal satiety leading to reduction in appetite and food intake (Q&A, 2009).The DB gene found in diabetes patient also stimulates the OB protein receptor leading to production of leptin, hence the link between diabetes and obesity.
In conclusion, obesity is really a genetic problem involving a lot of genetic diversity which makes its moral solution almost impossible. Article based on http://www.mrc.ac.uk/Newspublications/News/MRC004564

By SeoRin Park 41365654

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Genetically Mapping the Acne Bug

Acne, is a skin condition which many of us have faced at sometime. The appearance and development of acne is greatly assisted by Propinonibacterium, a bacteria which live in our hair follicles. Although, they are generally harmless when the hair follicles become overfilled with sebum, an oily secretion they aggravate the skin and aid the development of acne. As acne is a prevalent and quite psychologically harmful for many people, scientists have been constantly studying the disease in the last couple of years. German microbiologist Dr Holger Brueggemann and his research team recently mapped the genetic code of the Propinonibacterium. Interestingly, they found that it contains a plasmid which contains 2 333 genes which enable highly destructive properties which are aimed in breaking down the skin. They actually found that the Propinonibacterium has genes which encode for enzymes which are very similar to those in “flesh eating bacteria”. It even had genes which code for substances which destroy competitors.
Most current treatments and medication used to treat acne are based on killing Propinonibacterium or preventing blockage of the hair follicles. Unfortunately, like most antibiotic treatments, the bacteria has rapidly developed resistance to the antibiotic. So what this German research team is hoping to do from mapping genome of the Propinonibacterium is to gain a better and more in depth understanding of the organism to find a more effective cure for acne. As scientists have mapped the genome of the Propinonibacterium, there is not much let to discover about this organism and hence, should not be long till they find a better treatment for acne.

Articlebased on:
http://www.articlesbase.com/acne-articles/scientists-discover-genetic-makeup-of-acne-bacterium-1332831.html#

Other suggested readings-
http://archderm.ama-assn.org/cgi/content/extract/137/9/1250
http://www.highbeam.com/doc/1G1-107524610.html