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By Emma Patten-Hitt
NEW YORK, Mar 07 (Reuters Health) - Researchers have stumbled upon an anti-aging gene present in both yeast and roundworms, two diverse organisms, indicating that similar genes are likely to regulate the aging process in other organisms--perhaps even humans.
Dr. Leonard Guarente and colleagues from the Massachusetts Institute of Technology in Cambridge already knew that the gene called SIR2 determined the life span of yeast, and that adding an extra copy of the gene extended its life span. So they looked to see if they could find a similar gene in a type of roundworm, and whether the gene would function the same way.
Indeed, the C. elegans roundworms did have a similar version of the gene, and Guarente's team found that roundworms with an additional copy of the gene lived up to 50% longer than their one-copied counterparts.
"The remarkable thing is that the same gene regulates aging in yeast and roundworms," Guarente told Reuters Health. "The huge evolutionary divergence rendered it unlikely that SIR2 genes would be present in both organisms," he said. "This means that SIR2 is likely to regulate aging generally, including in mammals."
Writing in the March 8th issue of Nature, the study authors suggest that in both yeast and roundworms, the gene somehow links nutrient availability to aging.
According to Guarente, there are seven SIR2-related genes in humans. "I think that our findings suggest that they will regulate human aging," he said. "It remains to be discovered exactly what these genes do in people, but this really focuses our attention to one gene family," he added.
"By studying mammalian SIR2 genes, we hope to understand the processes that control human aging," Guarente said. "We may eventually be able to use this information to design drugs that confer health benefits to aging individuals."
In a related editorial, Dr. David Gems of University College London, UK, notes, "At the very least, it seems that some genetic determinants of longevity and (aging) are conserved across animal groups," which he predicts will encourage those studying aging in model organisms.
SOURCE: Nature 2001;410:154-155, 227-230.
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