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Cell. 2002 Apr 19;109(2):217-28.

Anosmin-1, defective in the X-linked form of Kallmann syndrome, promotes axonal branch formation from olfactory bulb output neurons.

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1
Unité de Génétique des Déficits Sensoriels, Centre National de la Recherche Scientifique, Unité de Recherche Associée 1968, Institut Pasteur, 25 rue du Dr Roux, F-75724 Paris cedex 15, France. nyani@pasteur.fr

Abstract

The physiological role of anosmin-1, defective in the X chromosome-linked form of Kallmann syndrome, is not yet known. Here, we show that anti-anosmin-1 antibodies block the formation of the collateral branches of rat olfactory bulb output neurons (mitral and tufted cells) in organotypic cultures. Moreover, anosmin-1 greatly enhances axonal branching of these dissociated neurons in culture. In addition, coculture experiments with either piriform cortex or anosmin-1-producing CHO cells demonstrate that anosmin-1 is a chemoattractant for the axons of these neurons, suggesting that this protein, which is expressed in the piriform cortex, attracts their collateral branches in vivo. We conclude that anosmin-1 has a dual branch-promoting and guidance activity, which plays an essential role in the patterning of mitral and tufted cell axon collaterals to the olfactory cortex.

PMID:
12007408
[Indexed for MEDLINE]
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