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

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Abstract

The process of neuronal migration is precisely regulated by different molecules during corticogenesis. The FAK (focal adhesion kinase) plays a critical role in embryogenesis and is involved in cell motility through focal adhesions, but the underlying mechanisms on inordinate expression are unclear. To investigate the effect of FAK overexpression on neuronal migration spatiotemporally, mice FAK was transfected into the neurons in vivo by electroporation. Results showed that exogenous FAK distributed in the cytoplasm (in vivo) and co-localized with vinculin (in vitro) and induced aberrant neuronal migration via phosphorylation of FAK at Tyr925 during cerebral cortex development. Meanwhile, FAK Y925F mutant also induced aberrant neuronal migration like inordinate FAK/GFP phenotype. All these results implied that FAK-induced abnormal phenotype depended on phosphorylation of FAK at Tyr925, and this demonstrated that the overexpression of FAK impaired neuronal migration through its phosphorylation and activity of FAK during corticogenesis.

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Abbreviations

TBST:

Tris buffered saline with tween-20

ECL:

Electrochemiluminescence

IUE:

In utero electroporation

MZ:

Marginal zone

UCP:

Upper cortical plate

DCP:

Down cortical plate

IZ:

Intermediate zone

VZ:

Ventricular zone

Pia:

Pia mater

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Funding

This work was supported by National Natural Science Foundation of China (number: 31572477) and Project of Henan University Science Research (number: 2015YBZR010).

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Authors

Contributions

LA and SZ designed research. LA performed all the experiments. WL helped to analyze data and write the manuscript. XH helped to perform in utero electroporation. WZ helped to perform WB.

Corresponding author

Correspondence to Shanting Zhao.

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The authors declare that they have no competing interests.

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An, L., Li, W., Hu, X. et al. Abundant Focal Adhesion Kinase Causes Aberrant Neuronal Migration Via Its Phosphorylation at Tyr925. J Mol Neurosci 64, 102–110 (2018). https://doi.org/10.1007/s12031-017-1010-1

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  • DOI: https://doi.org/10.1007/s12031-017-1010-1

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