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Abundant Focal Adhesion Kinase Causes Aberrant Neuronal Migration Via Its Phosphorylation at Tyr925

Lei An1,2, Weiwei Li1, Xinde Hu1

  • 1College of Veterinary Medicine, Northwest A&F University, No.22 Xinong Road, Yangling, 712100, Shaanxi, People's Republic of China.

Journal of Molecular Neuroscience : MN
|December 7, 2017
PubMed

Insights

Overexpressing focal adhesion kinase (FAK) in developing mouse brains disrupts neuronal migration. This impairment is linked to FAK phosphorylation at Tyr925, highlighting its crucial role in corticogenesis.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Developmental Biology

Background:

  • Neuronal migration is crucial for brain development and is tightly regulated by molecular signals.
  • Focal adhesion kinase (FAK) is implicated in cell motility but its role in aberrant expression during corticogenesis is not fully understood.

Purpose of the Study:

  • To investigate the spatiotemporal effects of FAK overexpression on neuronal migration during cerebral cortex development.
  • To elucidate the specific mechanisms by which FAK influences neuronal positioning.

Main Methods:

  • In vivo electroporation of mouse FAK into developing neurons.
  • In vitro co-localization studies with vinculin.
  • Analysis of FAK phosphorylation at Tyr925 and its impact on neuronal migration.

Main Results:

  • Exogenous FAK was observed in the cytoplasm in vivo and co-localized with vinculin in vitro.
  • FAK overexpression led to aberrant neuronal migration during cerebral cortex development.
  • A FAK Y925F mutant also induced abnormal migration, indicating phosphorylation at Tyr925 is critical.

Conclusions:

  • FAK overexpression impairs neuronal migration in a manner dependent on its phosphorylation at Tyr925.
  • FAK activity, regulated by phosphorylation, plays a significant role in controlling neuronal positioning during corticogenesis.
Keywords:
Focal adhesion kinaseIn utero electroporationMutantNeuronal migrationPhosphorylation

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