Methionine Sulfoxide Reductase A Mediates Dietary Restriction-Induced Lifespan Extension in Caenorhabditis elegans
- *Corresponding Author:
- Kailiang Jia, Ph.D.
Department of Biological Sciences
Center for Molecular Biology and Biotechnology
Florida Atlantic University, 5353 Parkside Dr. Jupiter
FL 33458, USA
E-mail: [email protected]
Received date: September 04, 2013; Accepted date: September 24, 2013; Published date: September 26, 2013
Citation: Minnerly J, Zhang J, Aldunate R, Weissbach H, Jia K (2013) Methionine Sulfoxide Reductase A Mediates Dietary Restriction-Induced Lifespan Extension in Caenorhabditis elegans. Aging Sci 1: 110 doi:10.4172/2329-8847.1000110
Copyright: © 2013 Minnerly J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: Methionine sulfoxide reductase A (MsrA) is a well-studied antioxidant enzyme that has been found to be important for protecting cells against oxidative damage and regulating lifespan in several species. However, the role of MsrA in dietary restriction has not been examined. The authors evaluated the function of MsrA in dietary restriction-induced lifespan extension in Caenorhabditis elegans. Methods: C. elegans loss-of-function msra mutant animals and wild type control animals were subjected to two widely used dietary restriction treatments, solid dietary restriction (sDR) and dietary restriction by liquid bacteria (BDR). The survival of the animals was evaluated and the data was statistically analyzed. Results: The loss-of-function mutation of msra significantly suppressed the lifespan extension conferred by solid dietary restriction. By contrast, msra was dispensable for lifespan extension resulted from dietary restriction by diluted bacteria in liquid. Conclusion: msra-1 is a major factor in the sDR-induced lifespan extension. This result, coupled with the previous finding that MsrA mediates the effect of insulin-like signaling on lifespan extension, indicates an essential role of MsrA in the aging process in C. elegans.