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Long-lived yeast Courtesy of Valter Longo, USC
Friday, January 18th, 2008--
If you put baker's yeast on a diet and remove two of its genes it will live to the ancient age of 10 weeks, according to a study to appear in PLoS Genetics later this month. That's equivalent to 800 yeast years--ten times yeast's normal lifespan.
Restricting calories has been shown to prolong a mouse's life by about thirty percent; in yeast, diet alone can extend life-span two- or threefold, says the study's lead author, Valter Longo, professor in the Leonard Davis School of Gerontology at the University of Southern California in Los Angeles. This study identified three proteins that play a role in the life-extending effects of calorie restriction, but it's not yet clear exactly why diet prolongs life. "It has to do, in my opinion, with calorie distribution," Longo says. If you eat less, your body shifts its energy to anti-aging mechanisms, instead of growth and reproduction. This would allow an organism to weather a period of food scarcity, allowing the organism to reproduce when food becomes abundant again.
Gene manipulation is the other force at work in Longo's long-lived yeast. The tenfold increase in longevity only happened when two genes--RAS2 and SCH9--were removed from the yeast's DNA. Humans have similar genes that have been shown to be related to cancer, Longo says.
In a companion study out this week in the The Journal of Cell Biology, Longo and colleagues including Federica Madia, also from University of Southern California, show that these gene deletions can also serve as the antidote to an accelerated aging syndrome caused by the lack of an enzyme called RecQ helicase SGS1 in yeast.
If a fountain-of-youth for yeast doesn't seem relevant, Longo is also studying a human population isolated in the mountains of Ecuador that appears to have what he calls "equivalent mutations" to the genetically modified yeast. The humans have a mutation in their growth hormone receptor, which controls the genes that are analogous to those Longo dropped in yeast.
Ecuadorians homozygous for this mutation--meaning they have two copies of the growth hormone receptor mutation--don't live longer: in fact, they suffer from birth-defects. They are exceptionally small in stature and have a higher incidence of cardiovascular diseases (because a side effect of the mutation is increased fat storage). This may also be related to the theory that the genes cause the body to go into anti-aging mode, rather than reproductive mode, Longo says. In anti-aging mode, you would want to store fat to maintain you until the next time you are in growth mode.
But people who are heterozygous for this mutation--meaning they have one normal copy and one abnormal copy--have a normal stature and seem to be healthy, Longo says. "We're asking the question 'do they live longer, are they protected against cancer? Do we have a human population that is truly equivalent to the healthy long-lived mice and yeast that we, and others, have described.'"
--Flora Lichtman
Valter Longo
Albert L. and Madelyne G. Hanson Family Trust Associate Professor in Gerontology
University of Southern California
Los Angeles, California
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