The nematode worm Caenorhabditis elegans is a model system for the stu
dy of the genetic basis of aging. Maternal-effect mutations in four ge
nes-clk-1, clk-2, clk-3, and gro-1-interact genetically to determine b
oth the duration of development and life-span. Analysis of the phenoty
pes of these mutants suggests the existence of a general physiological
clock in the worm. Mutations in certain genes involved in dauer forma
tion (an alternative larval stage induced by adverse conditions in whi
ch development is arrested) can also extend life-span, but the life ex
tension of Clock mutants appears to be independent of these genes. The
daf-2(e1370) clk-1(e2519) worms, which carry life-span-extending muta
tions from two different pathways, live nearly five times as long as w
ild-type worms.