Each of the 23 genes somehow normally acts to reduce longevity, whereas inhibiting any one of them increases lifespan. For example, the worm's lifespan doubles when one gene is prohibited from working properly, and inhibition of another gene increases the length of life by 20%.
The genes discovered affect a wide variety of activities, including insulin signaling, metabolism, and dietary regulation. Genes involved in insulin signaling are particularly interesting because corresponding human genes could potentially play a role in diabetes and cancer, according to senior author Cynthia Kenyon, of the University of California, San Francisco, and her coauthors.
Citation: Hansen M, Hsu AL, Dillin A, Kenyon C (2005) New genes tied to endocrine, metabolic, and dietary regulation of lifespan from a Caenorhabditis elegans genomic RNAi screen. PLoS Genet 1(1): e17.
University of California, San Francisco
600 16th Street Rm S314
San Francisco, CA USA 94143-2200
Announcing the debut of a new open-access journal from the Public Library of Science - PLoS Genetics
The Public Library of Science (PLoS) is pleased to announce the July 25 launch of PLoS Genetics (http://www.
Genetics and genomics research has grown at a bewildering pace in the past 15 years. PLoS Genetics reflects the interdisciplinary nature of the field, and the research featured in the inaugural issue ranges from nematodes to humans and from cancer to evolution. Each research article is accompanied by a summary that places the findings in a broader context.
"The vision we have for PLoS Genetics as a community resource is first and foremost to support the dissemination of our science in a way that draws attention to the quality, depth, and scope of our best work. That this is an open-access journal is an integral part of this vision," the editorial team says. Open access--free availability and unrestricted use¬--to all articles published in the journal is central to the mission of PLoS Genetics and the Public Library of Science.
PLEASE MENTION PLoS Genetics (http://www.