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Folate acts in E. coli to accelerate C. elegans aging independently of bacterial biosynthesis.

Virk, B. and Jia, J. and Maynard, C.A. and Raimundo, A. and Lefebvre, J. and Richards, S.A. and Chetina, N. and Liang, Y. and Helliwell, N. and Cipinska, M. and Weinkove, D. (2016) 'Folate acts in E. coli to accelerate C. elegans aging independently of bacterial biosynthesis.', Cell reports., 14 (7). pp. 1611-1620.

Abstract

Folates are cofactors for biosynthetic enzymes in all eukaryotic and prokaryotic cells. Animals cannot synthesize folate and must acquire it from their diet or microbiota. Previously, we showed that inhibiting E. coli folate synthesis increases C. elegans lifespan. Here, we show that restriction or supplementation of C. elegans folate does not influence lifespan. Thus, folate is required in E. coli to shorten worm lifespan. Bacterial proliferation in the intestine has been proposed as a mechanism for the life-shortening influence of E. coli. However, we found no correlation between C. elegans survival and bacterial growth in a screen of 1,000+ E. coli deletion mutants. Nine mutants increased worm lifespan robustly, suggesting specific gene regulation is required for the life-shortening activity of E. coli. Disrupting the biosynthetic folate cycle did not increase lifespan. Thus, folate acts through a growth-independent route in E. coli to accelerate animal aging.

Item Type:Article
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Status:Peer-reviewed
Publisher Web site:http://dx.doi.org/10.1016/j.celrep.2016.01.051
Publisher statement:This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
Record Created:12 Feb 2016 13:05
Last Modified:30 Mar 2016 16:04

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