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Engulfing cells promote neuronal regeneration and remove neuronal debris through distinct biochemical functions of CED-1

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  • Hui Chiu

    (University of Illinois at Chicago
    National Taiwan University
    California Institute of Technology)

  • Yan Zou

    (University of Illinois at Chicago
    ShanghaiTech University)

  • Nobuko Suzuki

    (University of Illinois at Chicago)

  • Yi-Wen Hsieh

    (University of Illinois at Chicago)

  • Chiou-Fen Chuang

    (University of Illinois at Chicago)

  • Yi-Chun Wu

    (National Taiwan University
    Academia Sinica)

  • Chieh Chang

    (University of Illinois at Chicago)

Abstract

Two important biological events happen coincidently soon after nerve injury in the peripheral nervous system in C. elegans: removal of axon debris and initiation of axon regeneration. But, it is not known how these two events are co-regulated. Mutants of ced-1, a homolog of Draper and MEGF10, display defects in both events. One model is that those events could be related. But our data suggest that they are actually separable. CED-1 functions in the muscle-type engulfing cells in both events and is enriched in muscle protrusions in close contact with axon debris and regenerating axons. Its two functions occur through distinct biochemical mechanisms; extracellular domain-mediated adhesion for regeneration and extracellular domain binding-induced intracellular domain signaling for debris removal. These studies identify CED-1 in engulfing cells as a receptor in debris removal but as an adhesion molecule in neuronal regeneration, and have important implications for understanding neural circuit repair after injury.

Suggested Citation

  • Hui Chiu & Yan Zou & Nobuko Suzuki & Yi-Wen Hsieh & Chiou-Fen Chuang & Yi-Chun Wu & Chieh Chang, 2018. "Engulfing cells promote neuronal regeneration and remove neuronal debris through distinct biochemical functions of CED-1," Nature Communications, Nature, vol. 9(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-07291-x
    DOI: 10.1038/s41467-018-07291-x
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