Longevity is a remarkably plastic trait, governed by genetic programs that enable organisms to respond appropriately to environmental cues. These genetic programs are highly conserved and were first discovered in model organisms such as yeast, worms, and flies. Germline-less and daf-2 insulin/IGF-1 signaling (IIS) mutants remain youthful and live longer than wild-type C. elegans. The conserved FOXO family transcription factor DAF-16 is required for germline-less and daf-2 longevity, and regulates expression of stress response, antimicrobial, and metabolic genes, and polymorphisms in both the IGF-1 receptor and FOXO are associated with human longevity. We recently discovered a novel, third state of longevity: when Caenorhabditis females mate, they shrink up to 30% and die soon after producing their last progeny, shortening their lifespan by 50%. Male sperm induces female germline proliferation and subsequent shrinking through the DAF-12/NHR control of osmotic regulation, and seminal fluid separately regulates DAF-16/FOXO nuclear exit and lifespan shortening. The shrinking signal is dynamic, and correlates with proliferation of germline stem cells. This remarkable phenomenon is not only a characteristic of C. elegans hermaphrodite mating, as species with true females (e.g., C. remanei) also undergo shrinking and death after mating. Thus, for gonochoristic species, which must mate to reproduce, such a fate is unavoidable. These effects are species-restricted. Female Caenorhabditis also exhibit profound changes in their behavior – and in males’ behavior toward them – after mating, in addition to the physiological changes that result in death immediately after producing a male's offspring.
Lunch @ 11:45, talk at 12pm.