It has long been assumed that the aging process is stochastic, beginning early in life and eventually gaining enough activity to cause the eventual decline and death of an organism. In contrast, aging can be viewed as a developmental process, much like early embryonic development, involving signals, receptive cues and timely action of these processes during discrete periods of an animal's life cycle. I have tested these opposing theories by determining when several genes required for lifespan extension actually function. Aging in C. elegans is regulated by a subset of genes that form a signal transduction pathway.
daf-2 is an insulin-like receptor that acts upstream of a PI3-kinase,
age-1. Both genes normally function to limit life span by down regulating the activity of
daf-16, a Forkhead-like transcription factor.
daf-16 normally functions to increase life span. I will present data indicating that the aging function of the genes
age-1,
daf-2 and
daf-16 is exerted during a specific period of the worm's life cycle. These results suggest that aging, at least in C. elegans, is regulated during specific periods in life. In addition, I have also started work on a novel screen to identify other genes required for life span regulation. Once these genes are identified I will test when they function.