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Cell Death Differ. 2005 Feb;12(2):153-61.

C. elegans ced-13 can promote apoptosis and is induced in response to DNA damage.

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1
Max-Planck-Institute of Biochemistry, Am Klopferspitz 18A, 82152 Martinsried, Germany.

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  • Cell Death Differ. 2005 May;12(5):532.

Abstract

The p53 tumor suppressor promotes apoptosis in response to DNA damage. Here we describe the Caenorhabditis elegans gene ced-13, which encodes a conserved BH3-only protein. We show that ced-13 mRNA accumulates following DNA damage, and that this accumulation is dependent on an intact C. elegans cep-1/p53 gene. We demonstrate that CED-13 protein physically interacts with the antiapoptotic Bcl-2-related protein CED-9. Furthermore, overexpression of ced-13 in somatic cells leads to the death of cells that normally survive, and this death requires the core apoptotic pathway of C. elegans. Recent studies have implicated two BH3-only proteins, Noxa and PUMA, in p53-induced apoptosis in mammals. Our studies suggest that in addition to the BH3-only protein EGL-1, CED-13 might also promote apoptosis in the C. elegans germ line in response to p53 activation. We propose that an evolutionarily conserved pathway exists in which p53 promotes cell death by inducing expression of two BH3-only genes.

PMID:
15605074
DOI:
10.1038/sj.cdd.4401539
[Indexed for MEDLINE]
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