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Losses of long-established genes contribute to human evolution

12-13-2007 · EurekAlert!

While it is well understood that the evolution of new genes leads to adaptations that help species survive, gene loss may also afford a selective advantage. A group of scientists at the University of California-Santa Cruz led by biomolecular engineering professor David Haussler has investigated this less-studied idea, carrying out the first systematic computational analysis to identify long-established genes that have been lost across millions of years of evolution leading to the human species.

Keywords: losses, long-established, genes, contribute, human, evolution, losse, long, established, gene

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Advance in understanding of blood pressure gene could lead to new treatments
02-04-2007 · EurekAlert!
Research by scientists at UCL (University College London) has clearly demonstrated for the first time the structure and function of a gene crucial to the regulation of blood pressure. The discovery could be important in the search for new treatments for illnesses such as heart disease, the UK's biggest killer. In a paper published online today in Nature Medicine, the team, led by Professor Patrick Vallance and Dr James Leiper, UCL Department of Medicine, reveal the role of the human gene dimethylarginine dimethylaminohydrolase (DDAH), showing that loss of DDAH activity disrupts nitric oxide (NO) production. NO is critical in the regulation of blood pressure, nervous system functions and the immune system. The role of DDAH is to break down modified amino acids (Asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA)) that are produced by the body and have been shown to inhibit NO synthase. These molecules accumulate in various disease states including diabetes, renal failure and pulmonary and systemic hypertension, and their concentration in plasma (the fluid component of blood) is strongly predicative of cardiovascular disease and death. In a healthy human body, the majority of ADMA is eliminated through active metabolism by DDAH. Scientists have hypothesised that if DDAH function is impaired, NO production is reduced, and that this could be an important feature of increased cardiovascular risk. To examine this pathway in more detail, the researchers deleted the DDAH gene in mice. These mice went on to develop hypertension, or high blood pressure. They also designed specific inhibitors (small molecules) which bind to the active site of human DDAH. These small molecule inhibitors also induced hypertension in mice, confirming the importance of DDAH in the regulation of blood pressure. Dr Leiper, UCL Medicine, said: “These genetic and chemical approaches to disrupt DDAH showed remarkably consistent results, and provide compelling evidence that loss of DDAH function increases the concentration of ADMA and thereby disrupts vascular NO signalling. “There has been considerable scientific interest in this pathway and the role of ADMA as a novel risk factor, but so far there's been little evidence to support the idea that it's a cause of disease, rather than just a marker. Genes and their pathways are crucial to our understanding of cardiovascular disease and a better understanding of DDAH-1 could lead to important new treatments. “It could help us to establish if genetic variation predisposes certain people to these diseases, or whether environmental factors exert some of their effects through modulation of DDAH activity. “Our research also shows that this pathway could be harnessed therapeutically to limit production of NO in certain situations where too much nitric oxide is a bad thing; for example, hypotension and septic shock. These are some of the biggest problems in intensive care medicine and there is a huge unmet need for drug treatments.” The study, which was carried out at UCL's Rayne Institute, was funded by grants from the British Heart Foundation, the Wellcome Trust and the Medical Research Council. Professor Jeremy Pearson, Associate Medical Director of the British Heart Foundation, said: "The unexpected finding in the 1980s that a simple gas, nitric oxide (NO), is made by cells in the blood vessel wall and is a powerful control of blood vessel relaxation led to the award of the Nobel Prize in 1998 to its discoverers. "More recently, there has been increasing evidence that impairment of NO production is likely to be an important factor in the development of heart and circulatory disease, but the mechanisms responsible are not fully understood. "This study suggests for the first time that the loss of the activity of the enzyme DDAH-1 leads to reduced NO production and may cause heart and circulatory disease. These findings are likely to be important in the search for new ways to optimise the health of our blood vessels." ### Notes for Editors 1. For more information, please contact Ruth Metcalfe in the UCL Media Relations Office on tel: +44 (0)20 7679 9739, mobile: +44 (0)7990 675 947, out of hours: +44 (0)7917 271 364, e-mail: r.metcalfe@ucl.ac.uk2. 'Disruption of methylarginine metabolism impairs vascular homeostasis' is published in the February issue of the journal Nature Medicine. Advance online publication is embargoed to 18.00 GMT (13.00 US Eastern) Sunday 4 February 2007. Journalists can obtain copies of the paper by contacting the UCL Media Relations Office.3. The study was funded by the British Heart Foundation, the Wellcome Trust and the Medical Research Council. About UCL Founded in 1826, UCL was the first English university established after Oxford and Cambridge, the first to admit students regardless of race, class, religion or gender, and the first to provide systematic teaching of law, architecture and medicine. In the government's most recent Research Assessment Exercise, 59 UCL departments achieved top ratings of 5* and 5, indicating research quality of international excellence. UCL is the fourth-ranked UK university in the 2006 league table of the top 500 world universities produced by the Shanghai Jiao Tong University. UCL alumni include Mahatma Gandhi (Laws 1889, Indian political and spiritual leader); Jonathan Dimbleby (Philosophy 1969, writer and television presenter); Junichiro Koizumi (Economics 1969, Prime Minister of Japan); Lord Woolf (Laws 1954, Lord Chief Justice of England & Wales); Alexander Graham Bell (Phonetics 1860s, inventor of the telephone), and members of the band Coldplay.
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Gene found for rare disorder may reveal new pathway in mental retardation
02-05-2007 · EurekAlert!
Studying mutations that give rise to a rare genetic disease, genetics researchers have identified a novel biological pathway that may have a broader role during human development, potentially in cases of mental retardation and autism. An international team of researchers identified two genes that contribute to Cornelia deLange syndrome, a multisystem genetic disease that affects an estimated one in 10,000 children.
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Brown scientists map structure of DNA-doctoring protein complex
12-06-2006 · EurekAlert!
Mobile DNA, which inserts foreign genes into target cells, is a powerful force in the march of evolution and the spread of disease. Working with the lambda virus and E. coli bacteria, Brown University biologists have solved the structure of a six-protein complex critical to performing this gene-grafting surgery. The technique they developed could be used to reveal the structure of other critical protein complexes, landing the work on the cover of Molecular Cell.
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Human proteins evolving slowly thanks to multi-tasking genes
02-06-2007 · University of Bath
Many human proteins are not as good as they might be because the gene sequences that code for them have a double role which slows down the rate at which they evolve, according to new research from the Department of Biology & Biochemistry published in PLoS Biology.
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Newly identified mechanism for silencing genes points to possible anti-cancer strategies
05-16-2007 · EurekAlert!
Scientists are only beginning to appreciate the extraordinary degree of control exercised over every step of the gene-to-protein production process. Only about 10 percent of human genes, for example, are active in a given cell at a given time, with the remaining 90 percent silenced by a various mechanisms. In a just-published study in Nature, scientists report an important new gene-silencing mechanism that points to promising potential targets for anti-cancer interventions.
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Human proteins evolving slowly thanks to multitasking genes
02-05-2007 · EurekAlert!
Many human proteins are not as good as they might be because the gene sequences that code for them have a double role which slows down the rate at which they evolve, according to new research published in PLoS Biology.
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New protein implicated in autism
03-22-2007 · EurekAlert!
Autism is a common neurodevelopmental disorder characterized by severely impaired social, communicative, and behavioral functions. Although several genes are associated with autism, none lie in the region of human chromosome 7 associated with autism susceptibility. Now, a new study demonstrates that mice lacking CADPS2, which is encoded by a gene in the autism susceptibility region of human chromosome 7, exhibit autistic-like characteristics, leading to the suggestion that CADPS2 defects might predispose individuals to autism.
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Inherited individual variations influence patterns of gene shuffling
01-31-2008 · EurekAlert!
The first large-scale, high-resolution study of human genetic recombination has found remarkably high levels of individual variation in genetic exchange, the process by which parents pass on a mosaic-like mixture of their genes. The high-resolution enables the researchers to map out the precise location of where these genetic exchanges occur and assess the differences in recombination rates between individuals.
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From a lowly yeast, researchers divine a clue to human disease
12-07-2006 · EurekAlert!
Working with a common form of brewer's yeast, University of Wisconsin-Madison researchers have uncovered novel functions of a key protein that allow it to act as a master regulatory switch -- a control that determines gene activity and that, when malfunctioning in humans, may contribute to serious neurological disorders.
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Comparing chimp, human DNA
10-12-2006 · EurekAlert!
Most of the big differences between human and chimpanzee DNA lie in regions that do not code for genes, according to a new study. Instead, they may contain DNA sequences that control how gene-coding regions are activated and read.
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