Mena is required for neurulation and commissure formation

Citation
Lm. Lanier et al., Mena is required for neurulation and commissure formation, NEURON, 22(2), 1999, pp. 313-325
Citations number
59
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEURON
ISSN journal
08966273 → ACNP
Volume
22
Issue
2
Year of publication
1999
Pages
313 - 325
Database
ISI
SICI code
0896-6273(199902)22:2<313:MIRFNA>2.0.ZU;2-D
Abstract
Mammalian enabled (Mena) is a member of a protein family thought to link si gnal transduction pathways to localized remodeling of the actin cytoskeleto n. 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 p rojecting from interhemispheric cortico-cortical neurons are misrouted in e arly neonates, and failed decussation of the corpus callosum as well as def ects in the hippocampal commissure and the pontocerebellar pathway are evid ent in the adult. Mena-deficient mice that are heterozygous for a Profilin I deletion die in utero and display defects in neurulation, demonstrating a n important functional role for Mena in regulation of the actin cytoskeleto n.