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NYU scientists identify how development of different species uses same genes with distinct features

03-30-2007 · EurekAlert!

Biologists at New York University have identified how different species use common genes to control their early development and alter how these genes are used to accommodate their own features.

Keywords: nyu, scientists, identify, development, different, species, uses, same, genes, distinct, features, scientist, specy, use, gene, feature

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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.
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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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A molecular map for aging in mice
11-28-2007 · EurekAlert!
Researchers at the National Institute of Aging and Stanford University have used gene arrays to identify genes whose activity changes with age in 16 different mouse tissues. The study, published Nov. 30 in PLoS Genetics, uses a newly available database called AGEMAP to document the process of aging in mice at the molecular level. The work describes how aging affects different tissues in mice, and ultimately could help explain why lifespan is limited to just two years in mice.
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Individuals and populations differ in gene activity levels, not just genes
03-01-2007 · EurekAlert!
Much like how a person's genetic code differs from other individuals, the level at which those genes are activated in the body differs from one person to another, scientists have learned. And though some of those differences in gene activity are seen between different populations -- Asians versus Europeans, for instance -- more of those variations are due to individual-level factors, further obscuring the biological meaning of "race."
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Study of damaged gene gives insight into causes of mental illness
05-02-2007 · EurekAlert!
Scientists have pinpointed how different types of damage in types of damage to the same gene can cause some people to suffer from schizophrenia while others have major depression.
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'Network' approach identifies potential breast cancer susceptibility gene
10-09-2007 · EurekAlert!
Like a crossword-puzzle solver who uses the letters in some answers to figure out others, researchers at Dana-Farber Cancer Institute and an international group of collaborators have used data on genes involved in inherited forms of breast cancer to identify a gene linked to non-hereditary cases of the disease.
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Innovative model connects circuit theory to wildlife corridors
12-20-2007 · EurekAlert!
Scientists at Northern Arizona University and the National Center for Ecological Analysis and Synthesis have developed a model that uses circuit theory to predict gene flow across landscapes. Their approach could give managers a better way to identify the best spots for wildlife corridors, which are crucial to protecting biodiversity.
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Children with gene show reduced cognitive function
11-05-2007 · EurekAlert!
Children possessing a gene known to increase Alzheimer's disease risk already show signs of reduced cognitive function, an Oregon Health & Science University study has found. Scientists discovered that 7- to 10-year-olds with a member of a family of genes implicated in development, nerve cell regeneration and neuroprotection display reduced spatial learning and memory, associated with later-life cognitive impairments. This suggests brain changes predisposing a person to Alzheimer's might occur much sooner than previously thought.
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Scientists find major susceptibility gene for Crohn's disease
04-15-2007 · EurekAlert!
Using a novel approach, researchers identified that the PHOX2B, NCF4 and ATG16L1 genes constitute genetic risk factors for Crohn's disease. In addition, their study identified two regions of the genome where genetic risk factors are located but no known genes were implicated -- further work will be necessary to identify the causal genes in these regions.
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U-M, Israeli scientists report major advance in search for genes associated with colon cancer
07-08-2007 · EurekAlert!
An international team of researchers is reporting on a 10-year study of colon cancer among Israeli Jews and Arabs. The researchers, led by a team from the University of Michigan Comprehensive Cancer Center, discovered a genetic marker that increased a person's risk of colon cancer by 23 percent. At the same time, three other research teams are reporting similar findings involving the same gene, strengthening the likelihood that this particular marker plays a role in colon cancer.
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