The Caenorhabditis elegans nicotinamidase PNC-1 enhances survival

被引：38

作者：

van der Horst, Armando ^{[1
]}

Schavemaker, Jolanda M. ^{[1
]}

Berkel, Wendy Pellis-van ^{[1
]}

Burgering, Boudewijn M. T. ^{[1
]}

机构：

[1] Univ Med Ctr Utrecht, Ctr Biomed Genet, Dept Physiol Chem, NL-3584 CG Utrecht, Netherlands

来源：

MECHANISMS OF AGEING AND DEVELOPMENT | 2007年 / 128卷 / 04期

关键词：

PNC-1; Sir2; DAF-16; nicotinamide; survival; stress; lifespan; aging;

D O I：

10.1016/j.mad.2007.01.004

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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. I 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. (C) 2007 Elsevier Ireland Ltd. All rights reserved.

引用

页码：346 / 349

页数：4

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