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Profilin and the Abl tyrosine kinase are required for motor axon outgrowth in the Drosophila embryo.

The ability of neuronal growth cones to be guided by extracellular cues requires intimate communication between signal transduction systems and the dynamic actin-based cytoskeleton at the leading edge. Profilin, a small, actin-binding protein, has been proposed to be a regulator of the cell motility machinery at leading edge membranes. However, its requirement in the developing nervous system has been unknown. Profilin associates with members of the Enabled family of proteins, suggesting that Profilin might link Abl function to the cytoskeleton. Here, genetic analysis in Drosophila is used to demonstrate that mutations in Profilin (chickadee) and Abl (abl) display an identical growth cone arrest phenotype for axons of intersegmental nerve b (ISNb). Moreover, the phenotype of a double mutant suggests that these components function together to control axonal outgrowth.

Pubmed ID: 10069335


  • Wills Z
  • Marr L
  • Zinn K
  • Goodman CS
  • Van Vactor D



Publication Data

February 30, 1999

Associated Grants

  • Agency: NINDS NIH HHS, Id: NS35909

Mesh Terms

  • Alleles
  • Animals
  • Axons
  • Contractile Proteins
  • Drosophila
  • Drosophila Proteins
  • Embryo, Nonmammalian
  • Microfilament Proteins
  • Motor Neurons
  • Mutation
  • Nervous System
  • Profilins
  • Proto-Oncogene Proteins c-abl