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

Christelle Forcet, Elke Stein, Laurent Pays, Véronique Corset, Fabien Llambi, Marc Tessier-Lavigne and Patrick Mehlen ()
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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

Nature, 2002, vol. 417, issue 6887, 443-447

Abstract: 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.

Date: 2002
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DOI: 10.1038/nature748

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