Similar molecular signals determine the pace of aging in yeast, flies, worms and possibly also in humans, according to three studies published today in the journal Science.
Earlier work had shown that in the roundworm Caenorhabditis elegans, a chain of signals triggered by an insulin-like hormone controls how long the worm will live. The hormone binds to a cell surface receptor called daf-2 and sets off a signal that, among other things, limits the worm's life span. Worms with certain mutations in the daf-2 gene or other genes in the chain live longer.
The new research reveals that certain mutations in the fruit fly equivalent of daf-2, a gene called InR, have a similar result: female flies carrying these mutations live almost twice as long as their normal counterparts, and males that make it past a certain age also survive longer. The reason for this, Marc Tatar of Brown University and his colleagues conclude, is that the InR mutation leads to a decrease in juvenile hormone, a regulator of aging.
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Likewise, altering an insulin-like hormone called CHICO lengthens the life span of flies¿especially females¿geneticist Linda Partridge of University College London and her colleagues report. And in the third study, Valter D. Longo of the University of Southern California and his team found that yeast cells with a mutation in a gene called SCH9, which resembles a player in the worm insulin signaling chain, live three times longer than normal cells.
What may tie these studies in simple organisms together with mammals is caloric restriction: Put on a constant diet, certain mammals live longer than normal. They also have lower levels of insulin in their blood, which suggests that their signaling chain is less active¿similar to that of the mutant worms, flies and yeast cells. Further research will tell if evolution has indeed conserved this mechanism of aging-control across so many different species.