Neuronal migrations and axon fasciculation are disrupted in ina-1 integrin mutants.
Integrins are heterodimeric cell surface receptors implicated in cell adhesion and signaling. Our analysis of C. elegans ina-1 alpha integrin mutants provides the first genetic evidence that migrating neurons require integrins. Mosaic analysis and expression studies show that ina-1 acts autonomously in cells to promote their migrations. Although axons generally extend to their normal targets in ina-1 mutants, bundling of axons into fascicles is defective, defining a previously unrecognized role for integrins. In addition to these neuronal phenotypes, ina-1 mutants also display many morphogenetic defects. Finally, we show that the C. elegans INA-1 alpha integrin subunit associates with the PAT-3beta subunit in vivo, suggesting that these proteins function together in cell migration, axon fasciculation, and morphogenesis.
Baum
P D
PD
Department of Molecular and Cell Biology, University of California, Berkeley 94720-3204, USA.
Garriga
G
G
D000818:Animals; D001369:Axons / Q000502:physiology*; D002465:Cell Movement / Q000235:genetics*; D016023:Integrins / Q000235:genetics*; D009154:Mutation / Q000235:genetics*; D009474:Neurons / Q000502:physiology*
D016023:Integrins