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Published online 1 November 2004. doi:10.1083/jcb.200403093
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 167, Number 3, 479-492
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Article

 The death receptor antagonist FAIM promotes neurite outgrowth by a mechanism that depends on ERK and NF-{kappa}B signaling

Carme Sole1,3, Xavier Dolcet3, Miguel F. Segura1,3, Humberto Gutierrez4, Maria-Teresa Diaz-Meco5, Raffaella Gozzelino1,3, Daniel Sanchis1,3, Jose R. Bayascas1, Carme Gallego2, Jorge Moscat5, Alun M. Davies4, and Joan X. Comella1,3

1 Group of Cell Signalling and Apoptosis, Department of Basic Medical Sciences, Universitat de Lleida, 25008 Lleida, Spain
2 Group of Cell Cycle, Department of Basic Medical Sciences, Universitat de Lleida, 25008 Lleida, Spain
3 Hospital Universitari Arnau de Vilanova, Laboratori de Recerca, 25198 Lleida, Spain
4 School of Biosciences, Cardiff University, Cardiff CF10 3US, Wales, UK
5 Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, 28049 Madrid, Spain

Correspondence to Joan X. Comella: joan.comella{at}cmb.udl.es

Fas apoptosis inhibitory molecule (FAIM) is a protein identified as an antagonist of Fas-induced cell death. We show that FAIM overexpression fails to rescue neurons from trophic factor deprivation, but exerts a marked neurite growth–promoting action in different neuronal systems. Whereas FAIM overexpression greatly enhanced neurite outgrowth from PC12 cells and sympathetic neurons grown with nerve growth factor (NGF), reduction of endogenous FAIM levels by RNAi decreased neurite outgrowth in these cells. FAIM overexpression promoted NF-{kappa}B activation, and blocking this activation by using a super-repressor I{kappa}B{alpha} or by carrying out experiments using cortical neurons from mice that lack the p65 NF-{kappa}B subunit prevented FAIM-induced neurite outgrowth. The effect of FAIM on neurite outgrowth was also blocked by inhibition of the Ras–ERK pathway. Finally, we show that FAIM interacts with both Trk and p75 neurotrophin receptor NGF receptors in a ligand-dependent manner. These results reveal a new function of FAIM in promoting neurite outgrowth by a mechanism involving activation of the Ras–ERK pathway and NF-{kappa}B.

X. Dolcet, M.F. Segura, and H. Gutierrez contributed equally to this paper.

A.M. Davies and J.X. Comella contributed equally to this paper.

Abbreviations used in this paper: DRG, dorsal root ganglion; ERK, extracellular regulated kinase; FAIM, Fas apoptosis inhibitory molecule; FasL, Fas ligand; P1, postnatal day; p75NTR, p75 neurotrophin receptor; SCG, superior cervical ganglion.


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