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

Ramanathan, SP; Helenius, J; Stewart, MP; Cattin, CJ; Hyman, AA; Muller, DJ

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

Ramanathan, SP Helenius, J Stewart, MP Cattin, CJ Hyman, AA Muller, DJ

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Publisher:: NATURE PUBLISHING GROUP
Publication Type:: Journal Article
Citation:: Nature cell biology, 2015, 17, (2), pp. 148-159
Issue Date:: 2015-02

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Field	Value	Language
dc.contributor.author	Ramanathan, SP
dc.contributor.author	Helenius, J
dc.contributor.author	Stewart, MP
dc.contributor.author	Cattin, CJ
dc.contributor.author	Hyman, AA
dc.contributor.author	Muller, DJ
dc.date.accessioned	2020-11-25T07:55:13Z
dc.date.available	2014-12-17
dc.date.available	2020-11-25T07:55:13Z
dc.date.issued	2015-02
dc.identifier.citation	Nature cell biology, 2015, 17, (2), pp. 148-159
dc.identifier.issn	1465-7392
dc.identifier.issn	1476-4679
dc.identifier.uri	http://hdl.handle.net/10453/144347
dc.description.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.
dc.format	Print-Electronic
dc.language	eng
dc.publisher	NATURE PUBLISHING GROUP
dc.relation.ispartof	Nature cell biology
dc.relation.isbasedon	10.1038/ncb3098
dc.rights	info:eu-repo/semantics/restrictedAccess
dc.subject	06 Biological Sciences, 11 Medical and Health Sciences
dc.subject.classification	Developmental Biology
dc.subject.mesh	Hela Cells
dc.subject.mesh	Intracellular Space
dc.subject.mesh	Humans
dc.subject.mesh	Cysteine
dc.subject.mesh	Microfilament Proteins
dc.subject.mesh	Actins
dc.subject.mesh	Myosin Type II
dc.subject.mesh	rho GTP-Binding Proteins
dc.subject.mesh	CDC2 Protein Kinase
dc.subject.mesh	Actomyosin
dc.subject.mesh	Fetal Proteins
dc.subject.mesh	Green Fluorescent Proteins
dc.subject.mesh	Nuclear Proteins
dc.subject.mesh	Microscopy, Atomic Force
dc.subject.mesh	Mitosis
dc.subject.mesh	Pressure
dc.subject.mesh	Models, Biological
dc.subject.mesh	Time Factors
dc.subject.mesh	rho-Associated Kinases
dc.subject.mesh	Actins
dc.subject.mesh	Actomyosin
dc.subject.mesh	CDC2 Protein Kinase
dc.subject.mesh	Cysteine
dc.subject.mesh	Fetal Proteins
dc.subject.mesh	Formins
dc.subject.mesh	Green Fluorescent Proteins
dc.subject.mesh	HeLa Cells
dc.subject.mesh	Humans
dc.subject.mesh	Intracellular Space
dc.subject.mesh	Microfilament Proteins
dc.subject.mesh	Microscopy, Atomic Force
dc.subject.mesh	Mitosis
dc.subject.mesh	Models, Biological
dc.subject.mesh	Myosin Type II
dc.subject.mesh	Nuclear Proteins
dc.subject.mesh	Pressure
dc.subject.mesh	Time Factors
dc.subject.mesh	rho GTP-Binding Proteins
dc.subject.mesh	rho-Associated Kinases
dc.title	Cdk1-dependent mitotic enrichment of cortical myosin II promotes cell rounding against confinement.
dc.type	Journal Article
utslib.citation.volume	17
utslib.location.activity	England
utslib.for	06 Biological Sciences
utslib.for	11 Medical and Health Sciences
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Strength - IBMD - Initiative for Biomedical Devices
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney
utslib.copyright.status	closed_access	*
dc.date.updated	2020-11-25T07:55:08Z
pubs.issue	2
pubs.publication-status	Published
pubs.volume	17
utslib.citation.issue	2

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.

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http://hdl.handle.net/10453/144347