Diet-Induced Developmental Acceleration Independent of TOR and Insulin in C. elegans

Dietary composition has major effects on physiology. Here, we show that developmental rate, reproduction, and lifespan are altered in C. elegans fed Comamonas DA1877 relative to those fed a standard E. coli OP50 diet. We identify a set of genes that change in expression in response to this diet and...

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Published inCell Vol. 153; no. 1; pp. 240 - 252
Main Authors MacNeil, Lesley T., Watson, Emma, Arda, H. Efsun, Zhu, Lihua Julie, Walhout, Albertha J.M.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 28.03.2013
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Summary:Dietary composition has major effects on physiology. Here, we show that developmental rate, reproduction, and lifespan are altered in C. elegans fed Comamonas DA1877 relative to those fed a standard E. coli OP50 diet. We identify a set of genes that change in expression in response to this diet and use the promoter of one of these (acdh-1) as a dietary sensor. Remarkably, the effects on transcription and development occur even when Comamonas DA1877 is diluted with another diet, suggesting that Comamonas DA1877 generates a signal that is sensed by the nematode. Surprisingly, the developmental effect is independent from TOR and insulin signaling. Rather, Comamonas DA1877 affects cyclic gene expression during molting, likely through the nuclear hormone receptor NHR-23. Altogether, our findings indicate that different bacteria elicit various responses via distinct mechanisms, which has implications for diseases such as obesity and the interactions between the human microbiome and intestinal cells. [Display omitted] ► Comamonas diet accelerates development in C. elegans even under dilute conditions ► Comamonas bacteria affect oscillating gene expression during development ► Developmental acceleration induced by Comamonas is independent of TOR and insulin ► NHR-23 is a candidate mediator of the dietary response Relative to the standard laboratory diet of E. coli, a diet of Comamonas bacteria accelerates worm development and reduces fecundity and lifespan. The developmental effect is due to a change in gene expression during the larval molting program via a mechanism that likely involves nuclear hormone receptors.
Bibliography:http://dx.doi.org/10.1016/j.cell.2013.02.049
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Current address: Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA
ISSN:0092-8674
1097-4172
DOI:10.1016/j.cell.2013.02.049