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GartnerAnton

Gartner, Anton
DNA Damage Response and Genetic Toxicology
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A conserved checkpoint pathway mediates DNA damage-induced apoptosis and cell cycle arrest in C. elegans

Author(s)
Gartner, AMilstein, SAhmed, SHodgkin, JHengartner, MO
Issued Date
2000-03
DOI
10.1016/S1097-2765(00)80438-4
URI
https://scholarworks.unist.ac.kr/handle/201301/30924
Fulltext
https://www.sciencedirect.com/science/article/pii/S1097276500804384?via%3Dihub
Citation
MOLECULAR CELL, v.5, no.3, pp.435 - 443
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.
Publisher
CELL PRESS
ISSN
1097-2765
Keyword
NEMATODE CAENORHABDITIS-ELEGANSHOMOLOGOUS CHROMOSOME SYNAPSISSACCHAROMYCES-CEREVISIAEMEIOTIC RECOMBINATIONPROTEIN CED-9DEATHGENEATMP53MEIOSIS

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