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Depletion of kinesin-12, amyosin-IIB-interacting protein, promotes migration of cortical astrocytes
Journal article   Open access   Peer reviewed

Depletion of kinesin-12, amyosin-IIB-interacting protein, promotes migration of cortical astrocytes

Jie Feng, Zunlu Hu, Haijiao Chen, Juan Hua, Ronghua Wu, Zhangji Dong, Liang Qiang, Yan Liu, Peter W. Baas and Mei Liu
Journal of cell science, v 129(12), pp 2438-2447
15 Jun 2016
PMID: 27170353
url
https://doi.org/10.1242/jcs.181867View
Published, Version of Record (VoR)Open Access (License Unspecified) Open

Abstract

Cell Biology Life Sciences & Biomedicine Science & Technology
Kinesin-12 (also named Kif15) participates in important events during neuronal development, such as cell division of neuronal precursors, migration of young neurons and establishment of axons and dendritic arbors, by regulating microtubule organization. Little is known about the molecular mechanisms behind the functions of kinesin-12, and even less is known about its roles in other cell types of the nervous system. Here, we show that kinesin-12 depletion from cultured rat cortical astrocytes decreases cell proliferation but increases migration. Co-immunoprecipitation, GST pulldown and small interfering RNA (siRNA) experiments indicated that kinesin-12 directly interacts with myosin-IIB through their tail domains. Immunofluorescence analyses indicated that kinesin-12 and myosin-IIB colocalize in the lamellar region of astrocytes, and fluorescence resonance energy transfer analyses revealed an interaction between the two. The phosphorylation at Thr1142 of kinesin-12 was vital for their interaction. Loss of their interaction through expression of a phosphorylation mutant of kinesin-12 promoted astrocyte migration. We suggest that kinesin-12 and myosin-IIB can form a hetero-oligomer that generates force to integrate microtubules and actin filaments in certain regions of cells, and in the case of astrocytes, that this interaction can modulate their migration.

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Cell Biology
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