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Phagocytosis promotes programmed cell death in C. elegans

Author

Listed:
  • Peter W. Reddien

    (Howard Hughes Medical Institute, 68-425, Massachusetts Institute of Technology)

  • Scott Cameron

    (Howard Hughes Medical Institute, 68-425, Massachusetts Institute of Technology
    Children's Hospital/Dana Farber Cancer Institute)

  • H. Robert Horvitz

    (Howard Hughes Medical Institute, 68-425, Massachusetts Institute of Technology)

Abstract

In the nematode Caenorhabditis elegans programmed cell death requires the killer genes egl-1, ced-4 and ced-3 (refs 1 and 2), and the engulfment of dying cells requires the genes ced-1, ced-2, ced-5, ced-6, ced-7, ced-10 and ced-12 (refs 3,4,5). Here we show that engulfment promotes programmed cell death. Mutations that cause partial loss of function of killer genes allow the survival of some cells that are programmed to die, and mutations in engulfment genes enhance the frequency of this cell survival. Furthermore, mutations in engulfment genes alone allow the survival and differentiation of some cells that would normally die. Engulfment genes probably act in engulfing cells to promote death, as the expression in engulfing cells of ced-1, which encodes a receptor that recognizes cell corpses6, rescues the cell-killing defects of ced-1 mutants. We propose that engulfing cells act to ensure that cells triggered to undergo programmed cell death by the CED-3 caspase7 die rather than recover after the initial stages of death.

Suggested Citation

  • Peter W. Reddien & Scott Cameron & H. Robert Horvitz, 2001. "Phagocytosis promotes programmed cell death in C. elegans," Nature, Nature, vol. 412(6843), pages 198-202, July.
    • Handle: RePEc:nat:nature:v:412:y:2001:i:6843:d:10.1038_35084096
    DOI: 10.1038/35084096
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    Cited by:

    1. Nadin Memar & Ryan Sherrard & Aditya Sethi & Carla Lloret Fernandez & Henning Schmidt & Eric J. Lambie & Richard J. Poole & Ralf Schnabel & Barbara Conradt, 2024. "The replicative helicase CMG is required for the divergence of cell fates during asymmetric cell division in vivo," Nature Communications, Nature, vol. 15(1), pages 1-17, December.

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