期刊
MECHANISMS OF AGEING AND DEVELOPMENT
卷 130, 期 10, 页码 670-680出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mad.2009.08.002
关键词
Oxidative stress; Caenorhabditis elegans; Protein L-isoaspartyl O-methyltransferase (pcm-1); Delay in development; Egg-laying defect (Egl)
资金
- USPHS Training Program [GM07185]
- USPHS [GM026020, AG032303]
We have shown that Caenorhabditis elegans lacking the PCM-1 protein repair L-isoaspartyl methyltransferase are more sensitive to oxidative stress than wild-type nematodes. Exposure to the redox-cycling quinone juglone upon exit from dauer diapause results in defective egg-laying (Egl phenotype) in the pcm-1 mutants only. Treatment with paraquat, a redox-cycling dipyridyl, causes a more severe developmental delay at the second larval stage in pcm-1 mutants than in wild-type nematodes. Finally, exposure to homocysteine and homocysteine thiolactone, molecules that can induce oxidative stress via distinct mechanisms, results in a more pronounced delay in development at the first larval stage in pcm-1 mutants than in wild-type animals. Homocysteine treatment also induced the Egl phenotype in mutant but not wild-type nematodes. All of the effects of these agents were reversed upon addition of vitamin C, indicating that the developmental delay and egg-laying defects result from oxidative stress. Furthermore, we have demonstrated that a mutation in the gene encoding the insulin-like receptor DAF-2 suppresses the Egl phenotype in pcm-1 mutants treated with juglone. Our results support a role of PCM-1 in the cellular responses mediated by the DAF-2 insulin-like signaling pathway in C. elegans for optimal protection against oxidative stress. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
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