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MBC in Press, published online ahead of print March 26, 2008
Mol. Biol. Cell 10.1091/mbc.E07-09-0947

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Submitted on September 20, 2007
Revised on March 17, 2008
Accepted on March 19, 2008

The Signaling Adaptor Protein CD3{zeta} Is a Negative Regulator of Dendrite Development in Young Neurons

Stéphane J. Baudouin,*{dagger}{ddagger} Julie Angibaud,*{dagger}{ddagger} Gildas Loussouarn,{ddagger}{sect}|| Virginie Bonnamain,*{dagger}{ddagger} Akihiro Matsuura,¶ Miyuki Kinebuchi,¶ Philippe Naveilhan,*{dagger}{ddagger} and Hélène Boudin*{dagger}{ddagger}

*INSERM, U643, Nantes, F44000 France; {dagger}CHU Nantes, Institut de Transplantation et de Recherche en Transplantation, ITERT, Nantes, F44000 France; {ddagger}Université de Nantes, Faculté de Médecine, Nantes, F44000 France; {sect}INSERM, U915, Nantes, F44000, France; ||CNRS, ERL3147, F-44000, France; Department of Pathology, Fujita Health University School of Medicine, Aichi, 470-1192, Japan

Monitoring Editor: Erika Holzbaur

A novel idea is emerging that a large molecular repertoire is common to the nervous and immune systems, which might reflect the existence of novel neuronal functions for immune molecules in the brain. Here, we show that the transmembrane adaptor signaling protein CD3{zeta}, first described in the immune system, has a previously uncharacterized role in regulating neuronal development. Biochemical and immunohistochemical analyses of the rat brain and cultured neurons showed that CD3{zeta} is mainly expressed in neurons. Distribution of CD3{zeta} in developing cultured hippocampal neurons, as determined by immunofluorescence, indicates that CD3{zeta} is preferentially associated with the somatodendritic compartment as soon as the dendrites initiate their differentiation. At this stage, CD3{zeta} was selectively concentrated at dendritic filopodia and growth cones, actin-rich structures involved in neurite growth and patterning. siRNA-mediated knockdown of CD3{zeta} in cultured neurons or overexpression of a loss-of-function CD3{zeta} mutant lacking the tyrosine phosphorylation sites in the ITAMs increased dendritic arborization. Conversely, activation of endogenous CD3{zeta} by a CD3{zeta} antibody reduced the size of the dendritic arbor. Altogether, our findings reveal a novel role for CD3{zeta} in the nervous system, suggesting its contribution to dendrite development through ITAM-based mechanisms.

Address correspondence to: Hélène Boudin (helene.boudin{at}univ-nantes.fr)






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