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Type I phosphatidylinositol 4‐phosphate 5‐kinase γ is required for neuronal migration in the mouse developing cerebral cortex
Author(s) -
Hara Yoshinobu,
Fukaya Masahiro,
Tamaki Hideaki,
Sakagami Hiroyuki
Publication year - 2013
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.12286
Subject(s) - microbiology and biotechnology , phosphatidylinositol , phosphatidylinositol 4,5 bisphosphate , focal adhesion , biology , electroporation , kinase , chemistry , signal transduction , biochemistry , gene
Type I phosphatidylinositol 4‐phosphate 5‐kinase ( PIP 5KI)γ is one of the phosphoinositide kinases that produce phosphatidylinositol 4,5‐bisphosphate, which is a critical regulator of cell adhesion formation, actin dynamics and membrane trafficking. Here, we examined the functional roles of PIP 5KIγ in radial neuronal migration during cortical formation. Reverse transcription–polymerase chain reaction analysis revealed that PIP 5KIγ_v2/v6 and PIP 5KIγ_v3 were expressed throughout cortical development with distinct expression patterns. In situ hybridisation analysis showed that PIP 5KIγ mRNA was expressed throughout the cortical layers. Immunohistochemical analysis revealed that PIP 5KIγ was localised in a punctate manner in the radial glia and migrating neuroblasts. Knockdown of PIP 5KIγ using in utero electroporation disturbed the radial neuronal migration and recruitment of talin and focal adhesion kinase to puncta beneath the plasma membrane. The same inhibitory effect on neuronal migration was observed by overexpression of a catalytically inactive mutant of PIP 5KIγ_v2 but not PIP 5KIγ_v1 or PIP 5KIγ_v3. These findings suggest an essential role of PIP 5KIγ, particularly PIP 5KIγ_i2, in neuronal migration, possibly through recruitment of adhesion components to the plasma membrane.