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Nat Cell Biol. 2015 Feb;17(2):148-59. doi: 10.1038/ncb3098. Epub 2015 Jan 26.

Cdk1-dependent mitotic enrichment of cortical myosin II promotes cell rounding against confinement.

Author information

1
Eidgenössische Technische Hochschule (ETH) Zurich, Department of Biosystems Science and Engineering, 4058 Basel, Switzerland.
2
1] Eidgenössische Technische Hochschule (ETH) Zurich, Department of Biosystems Science and Engineering, 4058 Basel, Switzerland [2] Massachusetts Institute of Technology (MIT), Department of Chemical Engineering, Cambridge, Massachusetts 02139, USA [3] The David H. Koch Institute for Integrative Cancer Research at MIT, Cambridge, Massachusetts 02139, USA.
3
Max Planck Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany.

Abstract

Actomyosin-dependent mitotic rounding occurs in both cell culture and tissue, where it is involved in cell positioning and epithelial organization. How actomyosin is regulated to mediate mitotic rounding is not well understood. Here we characterize the mechanics of single mitotic cells while imaging actomyosin recruitment to the cell cortex. At mitotic onset, the assembly of a uniform DIAPH1-dependent F-actin cortex coincides with initial rounding. Thereafter, cortical enrichment of F-actin remains stable while myosin II progressively accumulates at the cortex, and the amount of myosin at the cortex correlates with intracellular pressure. Whereas F-actin provides only short-term (<10 s) resistance to mechanical deformation, myosin sustains intracellular pressure for a longer duration (>60 s). Our data suggest that progressive accumulation of myosin II to the mitotic cell cortex probably requires the Cdk1 activation of both p21-activated kinases, which inhibit myosin recruitment, and of Rho kinase, which stimulates myosin recruitment to the cortex.

PMID:
25621953
DOI:
10.1038/ncb3098
[Indexed for MEDLINE]

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