Journal
SCIENTIFIC REPORTS
Volume 5, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/srep10449
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Funding
- Chinese 973 Project [2012CB945002, 2014CB964800]
- Ministry of Education [20113402130010, PCSIRT IRT13038]
- Anhui Project [08040102005]
- Chinese Natural Science Foundation [91313303, 31271518, 314300054, 31320103904]
- National Institutes of Health [CA164133, DK56292]
- Central University [WK2340000032, WK2340000021]
- BBSRC [BB/I021248/1]
- Wellcome Trust [090090/Z/09/Z]
- BBSRC [BB/I021248/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/I021248/1] Funding Source: researchfish
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Accurate chromosome segregation during mitosis requires the physical separation of sister chromatids which depends on correct position of mitotic spindle relative to membrane cortex. Although recent work has identified the role of PLK1 in spindle orientation, the mechanisms underlying PLK1 signaling in spindle positioning and orientation have not been fully illustrated. Here, we identified a conserved signaling axis in which NDR1 kinase activity is regulated by PLK1 in mitosis. PLK1 phosphorylates NDR1 at three putative threonine residues (T-7, T-183 and T-407) at mitotic entry, which elicits PLK1-dependent suppression of NDR1 activity and ensures correct spindle orientation in mitosis. Importantly, persistent expression of non-phosphorylatable NDR1 mutant perturbs spindle orientation. Mechanistically, PLK1-mediated phosphorylation protects the binding of Mob(1) to NDR1 and subsequent NDR1 activation. These findings define a conserved signaling axis that integrates dynamic kinetochore-microtubule interaction and spindle orientation control to genomic stability maintenance.
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