Consider, for instance, the mutations that control longevity in nematodes, which are the particular type of microscopic worms favored by modern researchers. These mutations, as Cynthia Kenyon and her colleagues from the University of California, San Francisco, reported in Nature in 1993, are in a gene that was known to regulate the passage of young worms into a state known as dauer that is similar to hibernation in mammals. The worms will enter this dauer state, explains Kenyon, only if they have insufficient food to survive. “The way these worms work,” she explains, “is that the worm hatches from the egg, and if there’s not a lot of food around, it goes through various larval stages and ends up in this dauer state…. It doesn’t eat or do anything else. Then, if you give it food, it will exit the state and reproduce and have a normal lifespan.” The particular genetic mutation that Kenyon discovered resulted in worms that lived twice as long as normal worms, and this was, at the time, the longest lifespan extension ever reported in an organism. Kenyon then demonstrated that this increased longevity was not simply a consequence of some kind of developmental arrest—as though the mutation had somehow trapped a young worm in a dauerlike limbo—but was actually the result of the mutation’s triggering a lifespan-extension mechanism in adult worms. In other words, this mutation was keyed into a genetic program that actually regulates longevity, and does it in a way that would be evolutionarily advantageous.

In 1997, the Harvard geneticist Gary Ruvkun reported that the gene in question was the single worm-equivalent of a trio of insulin-related genes in humans. In retrospect, this wasn’t surprising, noted Ruvkun, because here was a gene in worms that regulated a process—dauer—that depended on the presence or absence of food in the environment, and insulin and IGF are the genes in more sophisticated organisms that respond specifically to food availability. As it turns out, particularly long-lived fruit-fly mutants have also been found to have defects in this same insulin-like gene pathway, which serves to regulate in the fly a condition very similar to dauer and hibernation.