The nematode Caenorhabditis elegans responds to conditions of overcrowding and limited food by arresting development as a dauer larva. Genetic analysis of mutations that alter dauer larva formation (daf mutations) is presented along with an updated genetic pathway for dauer vs. nondauer development. Mutations in the
daf-2 and
daf-23 genes double adult life span, whereas mutations in four other dauer-constitutive genes positioned in a separate branch of this pathway (
daf-1,
daf-4,
daf-7 and
daf-8) do not. The increased life spans are suppressed completely by a
daf-16 mutation and partially in a
daf-2;
daf-18 double mutant. A genetic pathway for determination of adult life span is presented based on the same strains and growth conditions used to characterize Daf phenotypes. Both dauer larva formation and adult life span are affected in
daf-2;
daf-12 double mutants in an allele-specific manner. Mutations in
daf-12 do not extend adult life span, but certain combinations of
daf-2 and daf-le mutant alleles nearly quadruple it. This synergistic effect, which does not equivalently extend the fertile period, is the largest genetic extension of life span yet observed in a metazoan.