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J. Biol. Chem., Vol. 279, Issue 19, 19996-20001, May 7, 2004

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Lack of Peroxisomal Catalase Causes a Progeric Phenotype in Caenorhabditis elegans^*

Oleh I. Petriv and Richard A. Rachubinski, Canada Research Chair in Cell Biology and an International Research Scholar of the Howard Hughes Medical Institute

From the Department of Cell Biology, University of Alberta, Edmonton, Alberta T6G 2H7, Canada

Studies using the nematode Caenorhabditis elegans as a model system to investigate the aging process have implicated the insulin/insulin-like growth factor-I signaling pathway in the regulation of organismal longevity through its action on a subset of target genes. These targets can be classified into genes that shorten or extend life-span upon their induction. Genes that shorten life-span include a variety of stress response genes, among them genes encoding catalases; however, no evidence directly implicates catalases in the aging process of nematodes or other organisms. Using genetic mutants, we show that lack of peroxisomal catalase CTL-2 causes a progeric phenotype in C. elegans. Lack of peroxisomal catalase also affects the developmental program of C. elegans, since ctl-2 mutants exhibit decreased egg laying capacity. In contrast, lack of cytosolic catalase CTL-1 has no effect on either nematode aging or egg laying capacity. The ctl-2 mutation also shortens the maximum life-span of the long lived clk-1 mutant and accelerates the onset of its egg laying period. The more rapid aging of ctl-2 worms is apparently not due to increased carbonylation of the major C. elegans proteins, although altered peroxisome morphology in the ctl-2 mutant suggests that changes in peroxisomal function, including increased production of reactive oxygen species, underlie the progeric phenotype of the ctl-2 mutant. Our findings support an important role for peroxisomal catalase in both the development and aging of C. elegans and suggest the utility of the ctl-2 mutant as a convenient model for the study of aging and the human diseases acatalasemia and hypocatalasemia.

Received for publication, January 8, 2004 , and in revised form, March 2, 2004.

^* This work was supported by grants from the Canadian Institutes of Health Research (to R. A. R.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains four additional figures.

Supported by a Studentship from the Alberta Heritage Foundation for Medical Research.

To whom correspondence should be addressed: Dept. of Cell Biology, University of Alberta, Medical Sciences Bldg. 5-14, Edmonton, Alberta T6G 2H7, Canada. Tel.: 780-492-9868; Fax: 780-492-9278; E-mail: rick.rachubinski{at}ualberta.ca.

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