A conserved checkpoint pathway mediates DNA damage-induced apoptosis and cell cycle arrest in C. elegans

Gartner, A., Milstein, S., Ahmed, S., Hodgkin, J., Hengartner, M. O. (March 2000) A conserved checkpoint pathway mediates DNA damage-induced apoptosis and cell cycle arrest in C. elegans. Molecular Cell, 5 (3). pp. 435-443. ISSN 1097-2765

URL: http://www.ncbi.nlm.nih.gov/pubmed/10882129
DOI: 10.1016/S1097-2765(00)80438-4

Abstract

To maintain genomic stability following DNA damage, multicellular organisms activate checkpoints that induce cell cycle arrest or apoptosis. Here we show that genotoxic stress blocks cell proliferation and induces apoptosis of germ cells in the nematode C. elegans. Accumulation of recombination intermediates similarly leads to the demise of affected cells. Checkpoint-induced apoptosis is mediated by the core apoptotic machinery (CED-S/CED-4/CED-3) but is genetically distinct from somatic cell death and physiological germ cell death. Mutations in three genes-mrt-2, which encodes the C. elegans homolog of the S. pombe rad1 checkpoint gene, rad-5, and him-7-block both DNA damage-induced apoptosis and cell proliferation arrest. Our results implicate rad1 homologs in DNA damage-induced apoptosis in animals.

Item Type: Paper
Uncontrolled Keywords: NEMATODE CAENORHABDITIS-ELEGANS HOMOLOGOUS CHROMOSOME SYNAPSIS SACCHAROMYCES-CEREVISIAE MEIOTIC RECOMBINATION PROTEIN CED-9 DEATH GENE ATM P53 MEIOSIS
Subjects: organism description > animal > C elegans
bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification
organs, tissues, organelles, cell types and functions > cell types and functions > cell functions > apoptosis
organs, tissues, organelles, cell types and functions > cell types and functions > cell functions > cell cycle
CSHL Authors:
Communities: CSHL labs > Hengartner lab
Depositing User: Matt Covey
Date: March 2000
Date Deposited: 31 Jan 2014 20:16
Last Modified: 31 Jan 2014 20:16
Related URLs:
URI: http://repository.cshl.edu/id/eprint/29368

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