Neuronal migrations and axon fasciculation are disrupted in ina-1 integrin mutants

Neuron. 1997 Jul;19(1):51-62. doi: 10.1016/s0896-6273(00)80347-5.


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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Axons / physiology*
  • Cell Movement / genetics*
  • Integrins / genetics*
  • Mutation / genetics*
  • Neurons / physiology*


  • Integrins