Dietary restriction delays development, reduces fecundity, and increases lifespan. Here we provide evidence that maternal nutritional status influences provisioning of progeny. In C. elegans, dietary restriction increases progeny size (Harvey and Orbidans, PLOS ONE 2011). We show that progeny of mothers raised under dietary restriction are also buffered against growth-retarding effects of extended L1 arrest (see abstract of J. Jordan et. al.). This suggests that progeny of mothers who experienced limited food are better able to cope with extended starvation. The response to nutrient availability is plastic such that exposure to dietary restriction in late larvae and young adults but not young larvae influences progeny size. Insulin-like signaling plays an important role in regulating embryo size. Disruption of the insulin-like receptor
daf-2 in the soma results in larger embryos. Furthermore, mutations in
daf-2/InsR and
daf-16/FOXO abolish progeny size plasticity in liquid culture-based dietary restriction, with
daf-16 epistatic to
daf-2. This suggests that insulin-like signaling mediates the effects of dietary restriction on progeny size. We find that
skn-1 and
pha-4, two canonical regulators of lifespan extension associated with dietary restriction, are also essential for embryo size increase in an
eat-2 genetic model of dietary restriction on solid media. These findings reveal that while fecundity is decreased in conditions of limited nutrients, the size and starvation resistance of progeny are increased, suggesting that adults anticipate environmental conditions in progeny provisioning. Furthermore, regulation of progeny size requires some of the same genes and pathways controlling lifespan in response to dietary restriction, implying a common response regulates both aging and progeny provisioning.