Genetics & Molecular Biology
SHP-2, a common biological protein molecule, is central to placental growth and could hold the key to mitigating growth restriction of babies in the womb, according to research is published today in Endocrinology.
Daniel, who over at Genetic Future
does an outstanding job staying on top of the science, technology, and business of personal genomics, has scored three fascinating guest posts
about the mess of privacy and legal complications that come up when a personal genomics company goes bankrupt. When you get yourself genotyped by one of these companies, they get your data - and you should be concerned about where that data goes if the company goes under:
How may lives have you saved? I've maybe two or three to my credit. Norman Borlaug
needed people to estimate for him, with complex statistical formulations. The Wikipedia estimate is 245 million. That may be low.
You may know that correlation studies have shown that the risk of becoming obese is 2.5 times higher for those who have double copies of the best known risk gene for being overweight or obese, the FTO gene (fat mass and obesity associated).
New discoveries of that sort have led to a resurgence in concern that we may be slaves to our genes, but is that the case? No, in every study obesity still required high calorie consumption, especially fat. A low fat diet neutralizes the harmful effects of the gene.
Today is the 25th anniversary of the discovery of DNA fingerprinting. So has it done anything important, like given us a real understanding of how men and women communicate?
Well, no, but the University of Leicester Department of Genetics has revealed males and females at least communicate on the fundamental genetic level, an idea which counters scientific theory that the X and Y chromosomes - those that define the sexes - do not communicate at all.
In research published in the American Journal of Human Genetics, Zoë Rosser and colleagues say they have shown that exchange of DNA does occur between the X and Y in the regions previously thought to be completely isolated.
Researchers say they have identified a genetic variation in people with type 2 diabetes that affects how the body's muscle cells respond to the hormone insulin.
Previous studies have identified several genetic variations in people with type 2 diabetes that affect how insulin is produced in the pancreas. Today's study shows for the first time a genetic variation that seems to impair the ability of the body's muscle cells to use insulin to help them make energy.
Do you ever wonder how many harmful mutations you carry in your genome? Even if you've never worried about how much of a mutant you are, geneticists have spent a lot of time thinking about this issue. They are interested in a) how much genetic variation is out there, and b) how much of that is potentially harmful and connected to disease? This month's issue of Genome Research has some new research on an individual's personal mutational load.
After earning the ire of computational biologists
and network theorists
last week, it's time to get to the positive side of networks and systems biology. If you hadn't guessed it before, the name of this blog reflects my interest in complex biological systems. When I rant about networks and comp. bio., it's tough love, and I really have the best interests of the field at heart.
Every week you probably see papers ( here and elsewhere) reporting the discovery of new genetic variants that affect the risk of coronary artery disease and heart attacks.
It's an exciting time and the findings will undoubtedly lead to new biological insights into the mechanisms that cause heart attacks, which in turn may result in new types of treatments, but how much value is there to it individually now? Is 'personalized medicine' for heart attacks on the way?
In 1935 one of the founders of modern genetics, J. B. S. Haldane, studied men in London with the blood disease hemophilia and estimated that there would be a one in 50,000 incidence of mutations causing hemophilia in the gene affected – the equivalent of a mutation rate of perhaps one in 25 million nucleotides across the genome.
Others have measured rates at a few further specific genes or compared DNA from humans and chimpanzees to produce general estimates of the mutation rate expressed more directly in nucleotides of DNA.
16 scientists report today the first direct measurement of the general rate of genetic mutation at individual DNA letters in humans and show that those early estimates were spot on.