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DOE JGI plumbs termite guts to yield novel enzymes for better biofuel production

11-21-2007 · EurekAlert!

Termites may provide the biochemical means to a greener biofuel future. The bellies of these tiny beasts harbor a gold mine of microbes that have now been tapped as a rich source of enzymes for improving the conversion of biomass to valuable biofuels. The genomic sequencing and analysis of the termite gut microbes by the US Department of Energy Joint Genome Institute are highlighted in the Nov. 22 edition of the journal Nature.

Keywords: doe, jgi, plumbs, termite, guts, yield, novel, enzymes, biofuel, production, plumb, gut, enzyme

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Super-fermenting fungus genome sequenced
03-04-2007 · EurekAlert!
On the road to making biofuels more economically competitive with fossil fuels, there are significant potholes to negotiate. For cellulosic ethanol production, one major detour has being addressed with the characterization of the genetic blueprint of the fungus Pichia stipitis, by the U.S. Department of Energy Joint Genome Institute (DOE JGI) and collaborators at the U.S. Forest Service, Forest Products Laboratory. The research is featured in the March 4 advanced online publication of Nature Biotechnology.
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NIH scientists discover novel cause of iron overload in thalassemia disorders
08-30-2007 · EurekAlert!
Researchers at NIH have discovered a novel cause of iron overload in patients with thalassemia. According to the study, thalassemia patients overproduce a protein called GDF15, which suppresses the production of a liver protein, hepcidin, which in turn leads to an increase in the uptake of dietary iron in the gut. This finding has implications for iron metabolism in other diseases and may contribute to the future development of therapies for thalassemia.
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Researchers find plant protein that may aid biofuel production
04-27-2007 · EurekAlert!
In a breakthrough that could make the production of cellulosic ethanol less expensive, Cornell researchers have discovered a class of plant enzymes that potentially could allow plant materials used to make ethanol to be broken down more efficiently than is possible using current technologies.
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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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Penn researchers discover novel pathway for increasing 'good' cholesterol
08-08-2007 · EurekAlert!
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Oak Ridge leads DOE INCITE effort in 2008
01-17-2008 · Oak Ridge National Laboratory (ORNL)
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Protein sensor for fatty acid buildup in mitochondria
02-14-2007 · EurekAlert!
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Enzyme's second messenger contributes to cell overgrowth
09-26-2007 · EurekAlert!
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Researchers identify molecules with interesting anti-clotting properties
11-08-2007 · EurekAlert!
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Relative abundance of common microbes living in the gut may contribute to obesity
12-20-2006 · EurekAlert!
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