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Related Experiment Videos

Mena is required for neurulation and commissure formation.

L M Lanier1, M A Gates, W Witke

  • 1Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA.

Neuron
|March 9, 1999
PubMed
Summary

Mammalian enabled (Mena), a protein crucial for actin cytoskeleton remodeling, is essential for proper neuronal axon guidance. Mena deficiency leads to severe developmental defects, including misrouted axons and failed brain commissure formation.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Developmental Biology

Background:

  • Mammalian enabled (Mena) is a protein family member implicated in linking signal transduction to actin cytoskeleton remodeling.
  • Mena directly binds Profilin, an actin-binding protein that influences actin polymerization.
  • In neurons, Mena localizes to growth cone filopodia tips.

Purpose of the Study:

  • To investigate the functional role of Mena in neuronal development and actin cytoskeleton regulation.
  • To determine the consequences of Mena deficiency on axon guidance and brain development.

Main Methods:

  • Analysis of Mena-deficient mice.
  • Assessment of axonal projection and brain commissure formation in neonates and adults.
  • Examination of developmental defects in mice with combined Mena and Profilin I deficiencies.

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Main Results:

  • Mena-deficient mice exhibit misrouted axons in cortico-cortical projections.
  • Defects in corpus callosum, hippocampal commissure, and pontocerebellar pathways are observed in adult Mena-deficient mice.
  • Mice heterozygous for Mena and Profilin I deletions display embryonic lethality and neurulation defects.

Conclusions:

  • Mena plays a critical role in regulating the actin cytoskeleton during neuronal development.
  • Mena is essential for accurate axon guidance and the formation of major brain commissures.
  • The interaction between Mena and Profilin is vital for proper neurulation and embryonic development.