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The Journal of Neuroscience, September 17, 2003, 23(24):8526-8531

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BRIEF COMMUNICATION
Fas/Tumor Necrosis Factor Receptor Death Signaling Is Required for Axotomy-Induced Death of Motoneurons In Vivo

Gabriele Ugolini,¹ Cédric Raoul,¹ Anna Ferri,² Christine Haenggeli,² Yoichi Yamamoto,¹ Danièle Salaün,¹ Christopher E. Henderson,¹ Ann C. Kato,² Brigitte Pettmann,^1 * and Anne-Odile Hueber^3 *

¹Unitè Mixte de Recherche 382, Developmental Biology Institute of Marseille, Centre National de la Recherche Scientifique, Institut National de la Santèet de la Recherche Mèdicale, Universitè de la Mèditerranèe, Assistance Publique Marseille, Campus de Luminy-Case 907, France, ²Department of Pathology, Faculty of Medicine, Centre Mèdical Universitaire, University of Geneva, 1211 Geneva, Switzerland, and ³Institute of Signaling, Developmental Biology and Cancer Research, Centre National de la Recherche Scientifique Unitè Mixte de Recherche 6543, Centre A. Lacassagne, 06189 Nice, France

Activation of the Fas death receptor leads to the death of motoneurons in culture. To investigate the role of Fas in programmed cell death and pathological situations, we used several mutant mice deficient for Fas signaling and made a novel transgenic FADD-DN (FAS-associated death domain-dominant-negative) strain. In vitro, motoneurons from all of these mice were found to be resistant to Fas activation and to show a delay in trophic deprivation-induced death. During normal development in vivo, no changes in motoneuron survival were observed. However, the number of surviving motoneurons was twofold higher in animals deficient for Fas signaling after facial nerve transection in neonatal mice. These results reveal a novel role for Fas as a trigger of axotomy-induced death and suggest that the Fas pathway may be activated in pathological degeneration of motoneurons.

Key words: Fas; motoneuron; programmed cell death; FADD; facial nerve; axotomy

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Received April 14, 2003; revised July 7, 2003; accepted July 25, 2003.

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