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

A Gartner1, S Milstein, S Ahmed

  • 1Cold Spring Harbor Laboratory, New York 11724, USA.

Molecular Cell
|July 6, 2000
PubMed

Insights

Genotoxic stress triggers apoptosis in C. elegans germ cells via checkpoint activation. This DNA damage response is genetically distinct and involves rad1 homologs, crucial for animal DNA damage-induced apoptosis.

Area of Science:

  • Genetics
  • Molecular Biology
  • Developmental Biology

Background:

  • Multicellular organisms utilize cell cycle checkpoints to preserve genomic stability after DNA damage.
  • These checkpoints can trigger cell cycle arrest or apoptosis to eliminate compromised cells.

Purpose of the Study:

  • To investigate the mechanisms of DNA damage-induced apoptosis in germ cells of the nematode C. elegans.
  • To identify genes involved in the DNA damage response pathway in C. elegans.

Main Methods:

  • Genotoxic stress was applied to C. elegans.
  • Cell proliferation and apoptosis were monitored.
  • Mutations in specific genes (mrt-2, rad-5, him-7) were analyzed for their effects on the DNA damage response.
  • The core apoptotic machinery (CED-9/CED-4/CED-3) was examined.

Main Results:

  • Genotoxic stress blocks C. elegans germ cell proliferation and induces apoptosis.
  • Accumulation of recombination intermediates also leads to cell death.
  • Checkpoint-induced apoptosis utilizes the CED-9/CED-4/CED-3 pathway but is distinct from somatic and physiological germ cell death.
  • Mutations in mrt-2 (a rad1 homolog), rad-5, and him-7 disrupt both DNA damage-induced apoptosis and proliferation arrest.

Conclusions:

  • The rad1 checkpoint gene homolog (mrt-2) plays a critical role in DNA damage-induced apoptosis in C. elegans germ cells.
  • These findings implicate rad1 homologs in DNA damage-induced apoptosis across animal species.
  • The study highlights a specific genetic pathway for germ cell apoptosis in response to genotoxic stress.

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