KIF20A/MKLP2 regulates the division modes of neural progenitor cells during cortical development

Anqi Geng, Runxiang Qiu, Kiyohito Murai, Jiancheng Liu, Xiwei Wu, Heying Zhang, Henry Farhoodi, Nam Duong, Meisheng Jiang, Jiing-kuan Yee, Walter Tsark and Qiang Lu ()
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Anqi Geng: Beckman Research Institute of the City of Hope
Runxiang Qiu: Beckman Research Institute of the City of Hope
Kiyohito Murai: Beckman Research Institute of the City of Hope
Jiancheng Liu: Beckman Research Institute of the City of Hope
Xiwei Wu: Beckman Research Institute of the City of Hope
Heying Zhang: Beckman Research Institute of the City of Hope
Henry Farhoodi: Beckman Research Institute of the City of Hope
Nam Duong: Beckman Research Institute of the City of Hope
Meisheng Jiang: University of California, Los Angeles
Jiing-kuan Yee: Beckman Research Institute of the City of Hope
Walter Tsark: Beckman Research Institute of the City of Hope
Qiang Lu: Beckman Research Institute of the City of Hope

Nature Communications, 2018, vol. 9, issue 1, 1-16

Abstract: Abstract Balanced symmetric and asymmetric divisions of neural progenitor cells (NPCs) are crucial for brain development, but the underlying mechanisms are not fully understood. Here we report that mitotic kinesin KIF20A/MKLP2 interacts with RGS3 and plays a crucial role in controlling the division modes of NPCs during cortical neurogenesis. Knockdown of KIF20A in NPCs causes dislocation of RGS3 from the intercellular bridge (ICB), impairs the function of Ephrin-B–RGS cell fate signaling complex, and leads to a transition from proliferative to differentiative divisions. Germline and inducible knockout of KIF20A causes a loss of progenitor cells and neurons and results in thinner cortex and ventriculomegaly. Interestingly, loss of function of KIF20A induces early cell cycle exit and precocious neuronal differentiation without causing substantial cytokinesis defect or apoptosis. Our results identify a RGS–KIF20A axis in the regulation of cell division and suggest a potential link of the ICB to regulation of cell fate determination.

Date: 2018
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DOI: 10.1038/s41467-018-05152-1

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