Abstract
Hypomorphic mutants affecting the Drosophila insulin/IGF signal pathway are reported to increase longevity in females but not in males. To understand this sex-difference, we conducted a large-scale demographic study with three new isogenic strains of alleles at chico, the insulin-receptor substrate homologue. We verify that female dwarf homozygotes (ch1/ch1) and normal-sized heterozygotes (ch1/+) are long-lived, as originally reported. We find for the first time that male heterozygotes are long-lived relative to wildtype, by about 50%. The life span of male ch1/ch1 is similar to that of wildtype but these dwarf males age at a slow demographic rate. The levels of demographic frailty and of age-independent mortality are elevated in ch1/ch1 males, counteracting the effect of slow aging upon life expectancy. Mortality deceleration occurs amongst the oldest-old wildtype adults, as seen in many organisms. Remarkably, in similarly sized cohorts of male and female ch1/ch1 and of male ch1/+ mortality deceleration is absent. Mortality deceleration is a phenotype of chico.
