vhp-1 knock-down in developing animals significantly increased DAF- 16::GFP nuclear localization in intestinal cells (independently of its effects on development itself), while its knock-down in adults reduced it. Both the larval-stage increase in DAF-16 nuclear localization and the adult-stage decrease were suppressed by
kgb-1 disruption, observed in mutants carrying either the
kgb-1(
um3) allele (not shown) or the
kgb-1(
km21) allele. Furthermore, presenting the mirror image to
vhp-1 knock-down, knock-down of
kgb-1 (for two generations) caused approximately a twofold increase in the prevalence of intestinal DAF-16::GFP nuclear localization in adults, from 3% in control-treated animals to 8% in
kgb-1(RNAi) adults. Together, these results support a role for KGB-1 in age-dependent antagonistic modulation of DAF-16.