Two University of Colorado at Boulder researchers working with GenoPlex Inc. in Denver have identified a biological switch that controls lifespan in tiny worms, a finding that could have applications for mammals, including people.
The switch, known as DAF-16, is a protein that can either lengthen or shorten the lifespan in the eyelash-sized roundworm, C. elegans, said CU-Boulder psychology Professor Thomas Johnson. Johnson, who is a fellow in the universitys Institute for Behavioral Genetics, or IBG, said DAF-16 is a critical part of a complex signaling pathway that involves insulin and glucose.
IBG Research Associate and principal author Samuel Henderson and Johnson are publishing a paper Dec. 11 on the topic in the prestigious journal Current Biology. Henderson and Johnson both are associated with GenoPlex.
The key to DAF-16 is whether it penetrates the nucleus of cells, said Henderson. "When it does penetrate the nucleus, it appears to turn on a switch to lengthen roundworm lives."
The switch, which is controlled by food availability, temperature and stress, likely has a homologue, or similar protein, in mammals, including humans, said Johnson. Insulin released with glucose in humans goes up and stores more fat when they consume sugar, inhibiting DAF-16 to enter the nucleus of the cells. It is likely that the same process occurs in other animals, he said.
Henderson has identified a molecule that embodies a trade off, said Johnson. "If DAF-16 is on, it triggers less reproduction, more efficient cell repair and longer lives. On the other hand, if DAF-16 is off, the result is more reproduction, worse cell repair and a shortened lifespan," he said.
Johnson authored a milestone paper in 1990 in Science magazine showing that mutating a single gene in roundworms could double their lifespan -- the first researcher discovered the lifespan of an animal could be increased by genetic mutation. Since then, resear
Contact: Thomas Johnson
University of Colorado at Boulder