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Comments on Sandrof, Moses et al. (2013) International Worm Meeting "Persistent effects of starvation on multiple life history traits." (0)
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Sandrof, Moses, Jobson, Meghan, Jordan, James, & Baugh, Ryan (2013). Persistent effects of starvation on multiple life history traits presented in International Worm Meeting. Unpublished information; cite only with author permission.
Starvation during early human development can increase adult disease risk, but it is thought that epigenetic effects of starvation could be adaptive if famine persists. We wanted to know if C. elegans has a potentially adaptive epigenetic response to starvation. To address this question, we characterized the response to early larval starvation during L1 arrest. We found a variety of phenotypic effects following recovery from extended L1 arrest. Remarkably, some of these effects persist for multiple generations. Growth and development are delayed after extended starvation, producing smaller adults, and fertility is reduced, but heat resistance increases. Starvation causes a striking amount of phenotypic variation among isogenic individuals, and those that develop slowest are least fertile but most heat resistant. But do these observations reflect an adaptive response to starvation, perhaps involving an epigenetic fitness trade-off, or are they part of a pathological response? L1 arrest increases heat resistance within hours, and resistance persists but declines through larval development, persumably due to chaperone dilution. Slower growing animals retain resistance longer, suggesting that the primary effect of extended starvation is actually slow growth. Slow growth appears to result from impaired feeding - animals subjected to extended starvation have lower rates of pumping throughout development, they exhibit a grinding defect as evidenced by the presence of whole bacteria in the gut, and individuals with the lowest pumping rates at the L1 stage tend to grow slowest. It was also recently shown that tissue damage is evident in the gonad after extended L1 arrest, resulting in reduced fertility upon recovery. These observations suggest that the effects of extended starvation we have characterized are pathological in nature, stemming from irreversible damage incurred during starvation. However, the manner by which these effects are transmitted to progeny remains an open and interesting question under investigation.
Affiliation:
- Dept Biol, Duke Univ, Durham, NC.