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Mena is required for neurulation and commissure formation.

Mammalian enabled (Mena) is a member of a protein family thought to link signal transduction pathways to localized remodeling of the actin cytoskeleton. Mena binds directly to Profilin, an actin-binding protein that modulates actin polymerization. In primary neurons, Mena is concentrated at the tips of growth cone filopodia. Mena-deficient mice are viable; however, axons projecting from interhemispheric cortico-cortical neurons are misrouted in early neonates, and failed decussation of the corpus callosum as well as defects in the hippocampal commissure and the pontocerebellar pathway are evident in the adult. Mena-deficient mice that are heterozygous for a Profilin I deletion die in utero and display defects in neurulation, demonstrating an important functional role for Mena in regulation of the actin cytoskeleton.

Pubmed ID: 10069337

Authors

  • Lanier LM
  • Gates MA
  • Witke W
  • Menzies AS
  • Wehman AM
  • Macklis JD
  • Kwiatkowski D
  • Soriano P
  • Gertler FB

Journal

Neuron

Publication Data

February 30, 1999

Associated Grants

  • Agency: NIGMS NIH HHS, Id: GM53236
  • Agency: NICHD NIH HHS, Id: HD18655
  • Agency: NICHD NIH HHS, Id: HD28478

Mesh Terms

  • Animals
  • Animals, Newborn
  • Axons
  • Brain
  • Carrier Proteins
  • Contractile Proteins
  • Cytoskeletal Proteins
  • Embryo, Mammalian
  • Embryonic and Fetal Development
  • Gene Deletion
  • Growth Cones
  • Mice
  • Microfilament Proteins
  • Mutation
  • Nervous System
  • Profilins
  • Tissue Distribution