Authors: van der Horst A; Schavemaker JM; Pellis-van Berkel W; Burgering BM
Abstract: In yeast, increasing the copy number of the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase Sir2 extends lifespan, which can be inhibited by nicotinamide (Nam), the end-product of Sir2-mediated NAD-breakdown. Furthermore, the yeast pyrazinamidase/nicotinamidase PNC-1 can extend yeast lifespan by converting Nam. In Caenorhabditis elegans (C. elegans), increased dosage of the gene encoding SIR-2.1 also increases lifespan. Here, we report that knockdown of the C. elegans homologue of yeast PNC-1 as well as growing worms on Nam-containing medium significantly decreases adult lifespan. Accordingly, increased gene dosage of pnc-1 increases adult survival under conditions of oxidative stress. These data show for the first time the involvement of PNC-1/Nam in the survival of a multicellular organism and may also contribute to our understanding of lifespan regulation in mammals.
Keywords: Animals; Animals, Genetically Modified; Caenorhabditis elegans/*enzymology/*growth & development; Longevity/*physiology; Niacinamide/metabolism; Nicotinamidase/*physiology; Oxidative Stress/physiology
Journal: Mechanisms of ageing and development Volume: 128 Issue: 4 Pages: 346-9 Date: March 6, 2007 PMID: 17335870 |
van der Horst A, Schavemaker JM, Pellis-van Berkel W, Burgering BM (2007) The Caenorhabditis elegans nicotinamidase PNC-1 enhances survival. Mechanisms of ageing and development 128: 346-9.
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