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Article Dans Une Revue Molecular and Cellular Neuroscience Année : 2004

Semaphorin3A-induced receptor endocytosis during axon guidance responses is mediated by L1 CAM.

Résumé

During axon navigation, Semaphorin3A-induced growth cone retraction is correlated with endocytosis. Although its function remains elusive, we showed previously that the cell adhesion molecule of the immunoglobulin super family L1 associates with Neuropilin-1 (NP-1) the Sema3A-binding subunit of the receptor complex and is required for Sema3A to elicit axonal repulsive responses. We report here that upon Sema3A binding to NP-1, L1 and NP-1 are co-internalized through a clathrin-dependent mechanism mediated by L1. We show that in COS7 cells, L1/NP-1 endocytosis is correlated with a cell contraction similar to that observed with the Plexin (Plex)/NP-1 or Plex/NP1/L1 complexes. In neuronal cultures, a L1-mimetic peptide able to switch Sema3A repulsive responses to attraction blocks both endocytosis and growth cone collapse. Similarly, in the COS7 cell model, peptide application prevents both the Sema3-induced L1/NP-1 internalization and cell collapse. These studies demonstrate that the L1/NP-1 complex is able to confer a biological response to Sema3A with L1 mediating receptor internalization following ligand activation. They also reveal that endocytosis controlled by L1/NP-1 cis and trans interactions is pivotal in Sema3A-mediated axon guidance.

Dates et versions

hal-00180561 , version 1 (19-10-2007)

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Valérie Castellani, Julien Falk, Geneviève Rougon. Semaphorin3A-induced receptor endocytosis during axon guidance responses is mediated by L1 CAM.. Molecular and Cellular Neuroscience, 2004, 26 (1), pp.89-100. ⟨10.1016/j.mcn.2004.01.010⟩. ⟨hal-00180561⟩
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