Study Identifies Genetic Regions Linked With Migraine

The team identified 12 genetic regions associated with migraine susceptibility. Eight of these regions were found in or near genes known to play a role in controlling brain circuitries and two of the regions were associated with genes that are responsible for maintaining healthy brain tissue. The regulation of these pathways may be important to the genetic susceptibility of migraines.

Migraine is a debilitating disorder that affects approximately 14% of adults. Migraine has recently been recognized as the seventh disabler in the Global Burden of Disease Survey 2010 and has been estimated to be the most costly neurological disorder. It is an extremely difficult disorder to study because no biomarkers between or during attacks have been identified so far.

"This study has greatly advanced our biological insight about the cause of migraine," says Dr Aarno Palotie, from the Wellcome Trust Sanger Institute. "Migraine and epilepsy are particularly difficult neural conditions to study; between episodes the patient is basically healthy so it's extremely difficult to uncover biochemical clues.

"We have proven that this is the most effective approach to study this type of neurological disorder and understand the biology that lies at the heart of it."

The team uncovered the underlying susceptibilities by comparing the results from 29 different genomic studies, including over 100,000 samples from both migraine patients and control samples.

They found that some of the regions of susceptibility lay close to a network of genes that are sensitive to oxidative stress, a biochemical process that results in the dysfunction of cells.

The team expects many of the genes at genetic regions associated with migraine are interconnected and could potentially be disrupting the internal regulation of tissue and cells in the brain, resulting in some of the symptoms of migraine.

"We would not have made discoveries by studying smaller groups of individuals," says Dr Gisela Terwindt, co-author from Leiden University Medical Centre. "This large scale method of studying over 100,000 samples of healthy and affected people means we can tease out the genes that are important suspects and follow them up in the lab."

The team identified an additional 134 genetic regions that are possibly associated to migraine susceptibility with weaker statistical evidence. Whether these regions underlie migraine susceptibility or not still needs to be elucidated. Other similar studies show that these statistically weaker culprits can play an equal part in the underlying biology of a disease or disorder.

"The molecular mechanisms of migraine are poorly understood. The sequence variants uncovered through this meta-analysis could become a foothold for further studies to better understanding the pathophysiology of migraine" says Dr K?ri Stef?nsson, President of deCODE genetics.

"This approach is the most efficient way of revealing the underlying biology of these neural disorders," says Dr Mark Daly, from the Massachusetts General Hospital and the Broad Institute of MIT and Harvard. "Effective studies that give us biological or biochemical results and insights are essential if we are to fully get to grips with this debilitating condition.

"Pursuing these studies in even larger samples and with denser maps of biological markers will increase our power to determine the roots and triggers of this disabling disorder."

Source-Eurekalert

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Genetic 'Switches' Do Play Big Role in Human Evolution: Study

The study provides evidence for a 40-year-old hypothesis that regulation of genes must play an important role in evolution since there is little difference between humans and chimps in the proteins produced by genes.

Indeed, human and chimpanzee proteins are more than 99 percent identical.

The researchers showed that the number of evolutionary adaptations to the part of the machinery that regulates genes, called transcription factor binding sites, might be roughly equal to adaptations to the genes themselves.

"This is the most comprehensive and most direct analysis to date of the evolution of gene regulatory sequences in humans," said senior author Adam Siepel, Cornell associate professor of biological statistics and computational biology.

"It's taken these 40 years to get a clear picture of what's going on in these sequences because we haven't had the data until very recently," said Leonardo Arbiza, a postdoctoral researcher in Siepel's lab and the paper's lead author.

Less than 2 percent of the human genome - the complete set of genetic material - contains genes that code for proteins. In cells, these proteins are instrumental in biological pathways that affect an organism's health, appearance and behavior.

Much less is known about the remaining 98 percent of the genome; however, in the 1960s, scientists recognized that some of the non-protein coding DNA regulates when and where genes are turned on and off, and how much protein they produce. The regulatory machinery works when proteins called transcription factors bind to specific short sequences of DNA that flank the gene, called transcription factor binding sites, and by doing so, switch genes on and off.

Among the findings, the study reports that when compared with protein coding genes, binding site DNA shows close to three times as many "weakly deleterious mutations," that is, mutations that may weaken or make an individual more susceptible to disease, but are generally not severe. Weakly deleterious mutations exist in low frequencies in a population and are eventually weeded out over time. These mutations are responsible for many inherited human diseases.

While genes generally tend to resist change, a mutation occasionally leads to a favorable trait and increases across a population; this is called positive selection. By contrast, "transcription factor binding sites show considerable amounts of positive selection," said Arbiza, with evidence for adaptation in binding sites that regulate genes controlling blood cells, brain function and immunity, among others.

"The overall picture shows more evolutionary flexibility in the binding sites than in protein coding genes. This has important implications for how we think about human evolution and disease," said Siepel.

The study was published June 9 in Nature Genetics.

Source-ANI

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Scientists identify genetic risk for pulmonary fibrosis factor

Team, including doctors and scientists of the Faculty of the University of Colorado's watched medicine a fairly common variant of the mucin 5b gene, a protein that is a component of the produced by bronchial mucosa. This variant of the gene MUC5B is fairly common, pulmonary fibrosis is a disease rarely reported.

In a review of CT over 2 600 adults don't have a diagnosis of pulmonary fibrosis, the researchers found evidence of imaging of inflammation of the lungs and the scars in about 9% of the people over 50 years. In this age group, these abnormal results on computer tomography were significantly more common in people of 21 percent with the genetic variant of MUC5B.

What is important, final pulmonary fibrosis seen on CT scan has been strongly linked to the genetic variant of MUC5B. Although these anomalies do not necessarily indicate a disease that progresses, the presence of these abnormalities have been associated with more shortness of breath and cough as well as smaller lung sizes and capacity of oxygen transfer.

The results suggest that pulmonary fibrosis, which is a condition where the lung tissue becomes thickened, rigid and scarred, may be part of a syndrome less severe, much more common, but probably and could potentially be predicted on the basis of the genetic variant of MUC5B.

A paper describing the discovery was published recently in the New England Journal of Medicine.

Twenty-one authors share credit for the paper, including researchers from Brigham and Women hospital and Boston University.

Source-ANI

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More Than a Third of Young Adults in Mexico Have Genetic Risk of Obesity

by Kathy Jones on? May 25, 2013 at 8:13 PM Genetics & Stem Cells News A new study conducted by a University of Illinois researcher at the Universidad Aut?noma de San Luis Potos reveals that more than a third of Mexican young adults have a genetic predisposition for obesity.
"The students who inherited genetic risk factors from both parents were already 15? pounds heavier and 2 inches bigger around the waist than those who hadn't. They also had slightly higher fasting glucose levels," said Margarita Teran-Garcia, a U of I professor of food science and human nutrition.

In the study, 251 18- to 25-year-olds were tested for risk alleles on the FTO gene as part of the Up Amigos project, a collaboration of scientists at the U of I and the Mexican university. The researchers are following the 10,000 yearly applicants to the Universidad Aut?noma de San Luis Potosi to learn how changes in students' weight, body mass index (BMI), and eating and exercise habits affect their health over time.

According to Teran-Garcia, the FTO gene is associated with a predisposition to obesity, increased BMI, and increased waist circumference. These traits can in turn contribute to many health-related problems, including cardiovascular disease and diabetes.

Of the young adults tested in the study, 15 percent had inherited the genetic risk from both parents?in other words, they carried two copies of the risk allele. Another 20 percent had inherited risk from one parent, meaning they had one copy of the risk allele. Sixty-five percent of the students in the study did not carry the risk allele.

"If young people realize early that they have this predisposition, they can fight against it. If they are at risk for obesity, eating a healthy diet and getting regular exercise is even more important for them," Teran-Garcia said.

She noted that 85 percent of Hispanics in the United States are of Mexican origin.

Although FTO markers and analysis are available for large groups of Caucasians, Asians, and African-Americans, few studies have examined the effects of this gene in Mexican and Mexican- American populations.

"This is the first study to target young adults in Mexico, although one other study has followed older Mexican adults who had already been diagnosed with diabetes, obesity, and obesity-related diseases," she said.

Scientists hypothesize that "fat" genes may be influenced by epigenetic modifications, she said. "So even if you have this predisposition, you may be able to change the way those genes behave by eating the right foods and getting more exercise. These good habits are especially important for young people who have a genetic risk for obesity."

Source-Eurekalert

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New 1-step Genetic Engineering Technology

by Bidita Debnath on? May 26, 2013 at 11:22 AM Research News The workhorses of biotechnology, scientists are reporting that a new streamlined approach to genetic engineering drastically reduces the time and effort needed to insert new genes into bacteria.
Published in the journal ACS Synthetic Biology, the method paves the way for more rapid development of designer microbes for drug development, environmental cleanup and other activities.

Keith Shearwin and colleagues explain that placing, or integrating, a piece of the genetic material DNA into a bacterium's genome is critical for making designer bacteria. That DNA can give microbes the ability to churn out ingredients for medication, for instance, or substances that break down oil after a big spill. But current genetic engineering methods are time-consuming and involve many steps. The approaches have other limitations as well. To address those drawbacks, the researchers sought to develop a new, one-step genetic engineering technology, which they named "clonetegration," a reference to clones or copies of genes or DNA fragments.

They describe development and successful laboratory tests of clonetegration in E. coli and Salmonella typhimurium bacteria, which are used in biotechnology. The method is quick, efficient and easy to do and can integrate multiple genes at the same time. They predict that clonetegration "will become a valuable technique facilitating genetic engineering with difficult-to-clone sequences and rapid construction of synthetic biological systems."

Source-Eurekalert

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Largest Genetic Sequencing Study of Human Disease Completed By Researchers

The exact cause of these diseases - autoimmune thyroid disease, coeliac disease, Crohn's disease, psoriasis, multiple sclerosis and type 1 diabetes- is unknown, but is believed to be a complex combination of genetic and environmental factors. In each disease only a proportion of the heritability is explained by the identified genetic variants. The techniques used to date, have generally identified common (in the population) variants of weak effect.

In this study, using high-throughput sequencing techniques,a global team of scientists sought to identify new variants, including rare and potentially high risk ones, in 25 previously identified risk genes in a sample of nearly 42,000 individuals (24,892 with autoimmune disease and 17,019 controls).

It has been suggested - in the 'rare-variant synthetic genome-wide association hypothesis' - that a small number of rare variants in risk genes are likely to be a major cause of the heritability of these conditions.

However, the study published today in the journal Nature, suggests that the genetic risk of these diseases more likely involves a complex combination of hundreds of weak-effect variants which are each common in the population.

The authors estimate that rare variants in these risk genes account for only around three per cent of the heritability of these conditions that can be explained by common variants.

David van Heel, Professor of Gastrointestinal Genetics at Barts and The London School of Medicine and Dentistry at Queen Mary and director of the Barts and The London Genome Centre, led the study. He said: "These results suggests that risk for these autoimmune diseases is not due to a few high-risk genetic variations but seems rather due to a random selection from many common genetic variants which each have a weak effect.

"For each disease there are probably hundreds such variants and the genetic risk is likely to come from inheriting a large number of these variants from both parents. If this is the case then it may never be possible to accurately predict an individual's genetic risk of these common autoimmune diseases. However, the results do provide important information about the biological basis of these conditions and the pathways involved, which could lead to the identification new drug targets."

The research utilized high-throughput sequencing techniques performed at the Barts and The London Genome Centre and demonstrated for the first time that the sequencing can call genotypes as accurately as 'gold standard techniques' such as genotyping array platforms.

Additional laboratory work was carried out at the Blizard institute at Queen Mary.

Professor Richard Trembath, Vice Principal and Executive Dean for Health at Barts and The London School of Medicine and Dentistry, Queen Mary, and a co-author on the paper said: "The results prompt a re-assessment of the genetic architecture that determines risk for development of common auto-immune disorders and will fuel future careful assessment of regions of the human genome beyond those presently known to confer susceptibility to these important medical conditions."

Source-Eurekalert

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