ABL1 regulates spindle orientation in adherent cells and mammalian skin

Shigeru Matsumura, Mayumi Hamasaki, Takuya Yamamoto, Miki Ebisuya, Mizuho Sato, Eisuke Nishida and Fumiko Toyoshima ()
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Shigeru Matsumura: Institute for Virus Research, Kyoto University
Mayumi Hamasaki: Institute for Virus Research, Kyoto University
Takuya Yamamoto: Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku
Miki Ebisuya: CREST, Japan Science and Technology Agency, 4-1-8 Honcho
Mizuho Sato: Graduate School of Biological Sciences, Nara Institute of Science and Technology
Eisuke Nishida: CREST, Japan Science and Technology Agency, 4-1-8 Honcho
Fumiko Toyoshima: Institute for Virus Research, Kyoto University

Nature Communications, 2012, vol. 3, issue 1, 1-10

Abstract: Abstract Despite the growing evidence for the regulated spindle orientation in mammals, a systematic approach for identifying the responsible genes in mammalian cells has not been established. Here we perform a kinase-targeting RNAi screen in HeLa cells and identify ABL1 as a novel regulator of spindle orientation. Knockdown of ABL1 causes the cortical accumulation of Leu-Gly-Asn repeat-enriched-protein (LGN), an evolutionarily conserved regulator of spindle orientation. This results in the LGN-dependent spindle rotation and spindle misorientation. In vivo inactivation of ABL1 by a pharmacological inhibitor or by ablation of the abl1 gene causes spindle misorientation and LGN mislocalization in mouse epidermis. Furthermore, ABL1 directly phosphorylates NuMA, a binding partner of LGN, on tyrosine 1774. This phosphorylation maintains the cortical localization of NuMA during metaphase, and ensures the LGN/NuMA-dependent spindle orientation control. This study provides a novel approach to identify genes regulating spindle orientation in mammals and uncovers new signalling pathways for this mechanism.

Date: 2012
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:3:y:2012:i:1:d:10.1038_ncomms1634

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DOI: 10.1038/ncomms1634

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