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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-9/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.