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Netrin-1-mediated axon outgrowth requires deleted in colorectal cancer-dependent MAPK activation

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Listed:
  • Christelle Forcet

    (University of Lyon)

  • Elke Stein

    (Howard Hughes Medical Institute)

  • Laurent Pays

    (University of Lyon)

  • Véronique Corset

    (University of Lyon)

  • Fabien Llambi

    (University of Lyon)

  • Marc Tessier-Lavigne

    (Howard Hughes Medical Institute)

  • Patrick Mehlen

    (University of Lyon)

Abstract

Neuronal growth cones are guided to their targets by attractive and repulsive guidance cues1. In mammals, netrin-1 is a bifunctional cue, attracting some axons and repelling others2,3,4,5. Deleted in colorectal cancer (Dcc) is a receptor for netrin-1 that mediates its chemoattractive effect on commissural axons6,7, but the signalling mechanisms that transduce this effect are poorly understood. Here we show that Dcc activates mitogen-activated protein kinase (MAPK) signalling, by means of extracellular signal-regulated kinase (ERK)-1 and -2, on netrin-1 binding in both transfected cells and commissural neurons. This activation is associated with recruitment of ERK-1/2 to a Dcc receptor complex. Inhibition of ERK-1/2 antagonizes netrin-dependent axon outgrowth and orientation. Thus, activation of MAPK signalling through Dcc contributes to netrin signalling in axon growth and guidance.

Suggested Citation

  • Christelle Forcet & Elke Stein & Laurent Pays & Véronique Corset & Fabien Llambi & Marc Tessier-Lavigne & Patrick Mehlen, 2002. "Netrin-1-mediated axon outgrowth requires deleted in colorectal cancer-dependent MAPK activation," Nature, Nature, vol. 417(6887), pages 443-447, May.
    • Handle: RePEc:nat:nature:v:417:y:2002:i:6887:d:10.1038_nature748
    DOI: 10.1038/nature748
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