Cynthia Kenyon, PhD, director of the UCSF’s Larry L. Hillblom Center for the Biology of Aging, smiles a lot these days. And with good reason. She has aging cornered and she knows it. In less than 20 years, her once-crazy idea – that genes regulate aging – has not only gone mainstream, but spawned a huge field of research with giant conclaves and dozens of journal articles published every year.
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One of Kenyon’s lab rotation students – Ramon Tabtiang – in one of his very first experiments, picked a needle out of the haystack that is the C. elegans genome. In short, he found a mutant gene, dubbed daf-2, that made worms live twice as long. C. elegans was — and is — a favorite model for developmental biologists and geneticists because its simple structure and entire three-week life are easily scrutinized under the microscope.

Watching the mutant worms, says Kenyon, was like “witnessing a miracle.” Not only did these worms live longer, they retained good muscle tone, squirmed, sought food and stayed youthful. In comparison, normal, or wild, worms of the same two-week age were flabby, tattered and sedentary. They looked old. The message was clear. The rate of aging was not “fixed in stone,” after all. It could be slowed.

In the years since, Kenyon and her team have made more eye-popping discoveries, including the role of a companion gene, called daf-16, that controls on or off signals in still other genes. Learning more about the insulin pathway in which these genes operate helped her to understand a cascade of signals and responses as they reverberate through individual tissues.

Better yet, by using this information to tweak here and there in the worm genome, Kenyon and her laboratory colleagues have been able to extend a worm’s life up to six times the normal span, with no significant decline in vitality until late in life.