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Updated: Jul 16, 2026
An Anoxia-starvation Model for Ischemia/Reperfusion in C. elegans
Published on: March 11, 2014
The Caenorhabditis elegans nicotinamidase PNC-1 enhances survival
Armando van der Horst1, Jolanda M Schavemaker, Wendy Pellis-van Berkel
1Department of Physiological Chemistry, Centre for Biomedical Genetics, University Medical Center Utrecht, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands. A.A.vanderHorst-2@umcutrecht.nl
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.
