Persistent Life History Effects of Extended Starvation

Starvation during early human development produces epigenetic effects that could be adaptive if famine persists. We modeled the response to early starvation exposure in C. elegans using `L1 arrest,' a reversible developmental arrest in the first larval stage brought on by hatching in the absence of food. We found lifelong developmental effects following recovery from extended L1 arrest. Remarkably, some epigenetic effects persist for multiple generations. After extended starvation, development is delayed, producing smaller adults, fertility is reduced, and stress resistance increases. Starvation causes a striking amount of phenotypic variation among isogenic individuals, and those that develop slowest are least fertile and most stress resistant. However, increased stress resistance appears to be characteristic of recovering animals following any amount of L1 arrest but decreasing as the animal grows, possibly by size-dependent dilution. We assessed starved animals for signs of autophagy-related feeding defects and found low rates of pumping and feeding as well as grinding defects. A retrospective pumping assay revealed that after extended starvation, animals with lower pumping rates at the L1 stage tended to grow slower. Our work shows that environmental conditions and life history have transgenerational life history effects on several organismal traits, and that these traits appear to be rooted in nutrient-deprivation secondary to autophagy-related feeding defects. However, the manner by which these effects are transmitted transgenerationally remains an open and interesting question.