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Longevity Diet

Researchers unmask a gene that protects C. elegans from lifespan-shrinking metabolic byproducts.

Written byRina Shaikh-Lesko
| 2 min read

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ACCELERATED AGING: C. elegans whose alh-6 gene is impaired cannot convert 1-pyrroline-5-carboxylate (P5C) to glutamate, but the impact of this defect differs depending on diet. Worms fed the E. coli strain HT115 maintain low activity levels of PRODH, an enzyme that converts proline to P5C. In worms fed OP50 E. coli, PRODH activity increases, leading to an accumulation of P5C. These worms die sooner, perhaps because of an associated increase in reactive oxygen species.© KIMBERLY BATTISTA

The paper
S. Pang, S.P. Curran, “Adaptive capacity to bacterial diet modulates aging in C. elegans,” Cell Metabolism, 19:221-31, 2014.

Evidence that diet can profoundly affect aging is beginning to emerge, sometimes through targeted studies and other times by accident. While breeding mutant C. elegans worms for an unrelated experiment, Sean Curran and Shanshan Pang, a pair of researchers who study aging at the University of Southern California, noticed that certain mutant worms had considerably shorter life spans depending on their diet. The findings led the two to uncover a compensatory molecular mechanism for dealing with different menu items.

In the lab, C. elegans feeds on a variety of E. coli strains—most commonly, the B strain OP50 and the K-12 strain HT115. In an initial ...

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