To be sure, this is not an isolated discovery, but one of dozens of discoveries reported since the 1983 publication of
A method for the isolation of longevity mutants in the nematode Caenorhabditis elegans and initial results. That study remained inconclusive about the mechanism; the author Michael Klass believed the mutation was causing caloric restriction, which was known to extend longevity.
During that era, Cynthia Kenyon was beginning her post-doctoral research in longevity at MIT. In 1993 she published
A C. elegans mutant that lives twice as long as wild type.
When we began our studies of aging, in the early 1990s, one C. elegans gene that affected lifespan had been described, though it was poorly understood. When this gene was altered by a mutation, the animals lived 30-50% longer than normal. We looked for gene changes (mutations) that extended the lifespan of the roundworms, and we found that mutations in a gene called daf-2 doubled lifespan. These mutant worms still looked and acted young when they should be old. Seeing them is like being with someone that looks 40 and learning that they are really 80. This was a stunning finding because no one thought it was possible. We also discovered another important gene, called daf-16, that was needed for this long lifespan. daf-16 was a gene that could keep an animal young.
http://kenyonlab.ucsf.edu/html/non-scientist_overview.html
She will certainly go down as one of the pioneers in this field.
Considerable work has been done since Klaas and Kenyon broke ground. As of today there are 1825 genes identified as related to longevity according to the
GenAge database. Notice these are divided into findings from bacteria, yeast, roundworms, fruit flies, and mice.
