TY - JOUR
T1 - Mitosis-Specific Mechanosensing and Contractile-Protein Redistribution Control Cell Shape
AU - Effler, Janet C.
AU - Kee, Yee Seir
AU - Berk, Jason M.
AU - Tran, Minhchau N.
AU - Iglesias, Pablo A.
AU - Robinson, Douglas N N.
N1 - Funding Information:
We thank the members of the Robinson Lab for many helpful discussions and Sue Craig (Johns Hopkins) and Yixian Zheng (Carnegie Institution) for reading the manuscript. This work was supported by a Burroughs-Wellcome Career Development Award (D.N.R.), a Beckman Young Investigator Award (D.N.R.), the National Institutes of Health (R01#GM066817 to D.N.R., GM071920 to P.A.I.), and the National Science Foundation (DMS0083500 to P.A.I.).
PY - 2006/10/10
Y1 - 2006/10/10
N2 - Because cell-division failure is deleterious, promoting tumorigenesis in mammals [1], cells utilize numerous mechanisms to control their cell-cycle progression [2-4]. Though cell division is considered a well-ordered sequence of biochemical events [5], cytokinesis, an inherently mechanical process, must also be mechanically controlled to ensure that two equivalent daughter cells are produced with high fidelity. Given that cells respond to their mechanical environment [6, 7], we hypothesized that cells utilize mechanosensing and mechanical feedback to sense and correct shape asymmetries during cytokinesis. Because the mitotic spindle and myosin II are vital to cell division [8, 9], we explored their roles in responding to shape perturbations during cell division. We demonstrate that the contractile proteins myosin II and cortexillin I redistribute in response to intrinsic and externally induced shape asymmetries. In early cytokinesis, mechanical load overrides spindle cues and slows cytokinesis progression while contractile proteins accumulate and correct shape asymmetries. In late cytokinesis, mechanical perturbation also directs contractile proteins but without apparently disrupting cytokinesis. Significantly, this response only occurs during anaphase through cytokinesis, does not require microtubules, and is independent of spindle orientation, but is dependent on myosin II. Our data provide evidence for a mechanosensory system that directs contractile proteins to regulate cell shape during mitosis.
AB - Because cell-division failure is deleterious, promoting tumorigenesis in mammals [1], cells utilize numerous mechanisms to control their cell-cycle progression [2-4]. Though cell division is considered a well-ordered sequence of biochemical events [5], cytokinesis, an inherently mechanical process, must also be mechanically controlled to ensure that two equivalent daughter cells are produced with high fidelity. Given that cells respond to their mechanical environment [6, 7], we hypothesized that cells utilize mechanosensing and mechanical feedback to sense and correct shape asymmetries during cytokinesis. Because the mitotic spindle and myosin II are vital to cell division [8, 9], we explored their roles in responding to shape perturbations during cell division. We demonstrate that the contractile proteins myosin II and cortexillin I redistribute in response to intrinsic and externally induced shape asymmetries. In early cytokinesis, mechanical load overrides spindle cues and slows cytokinesis progression while contractile proteins accumulate and correct shape asymmetries. In late cytokinesis, mechanical perturbation also directs contractile proteins but without apparently disrupting cytokinesis. Significantly, this response only occurs during anaphase through cytokinesis, does not require microtubules, and is independent of spindle orientation, but is dependent on myosin II. Our data provide evidence for a mechanosensory system that directs contractile proteins to regulate cell shape during mitosis.
KW - CELLBIO
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U2 - 10.1016/j.cub.2006.08.027
DO - 10.1016/j.cub.2006.08.027
M3 - Article
C2 - 17027494
AN - SCOPUS:33749253712
SN - 0960-9822
VL - 16
SP - 1962
EP - 1967
JO - Current Biology
JF - Current Biology
IS - 19
ER -