| Autor: |
Chugh P; MRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK., Clark AG; MRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK., Smith MB; MRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK., Cassani DAD; MRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK., Dierkes K; Centre for Genomic Regulation, The Barcelona Institute of Science and Technology, Barcelona 08003, Spain.; Universitat Pompeu Fabra, Barcelona 08003, Spain., Ragab A; MRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK., Roux PP; Institute for Research in Immunology and Cancer, Université de Montréal, Montréal, Québec H3C 3J7, Canada., Charras G; London Centre for Nanotechnology, University College London, London WC1H 0AH, UK.; Department of Cell and Developmental Biology, University College London, London WC1E 6BT, UK., Salbreux G; The Francis Crick Institute, London NW1 1AT, UK., Paluch EK; MRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK. |
| Abstrakt: |
Animal cell shape is largely determined by the cortex, a thin actin network underlying the plasma membrane in which myosin-driven stresses generate contractile tension. Tension gradients result in local contractions and drive cell deformations. Previous cortical tension regulation studies have focused on myosin motors. Here, we show that cortical actin network architecture is equally important. First, we observe that actin cortex thickness and tension are inversely correlated during cell-cycle progression. We then show that the actin filament length regulators CFL1, CAPZB and DIAPH1 regulate mitotic cortex thickness and find that both increasing and decreasing thickness decreases tension in mitosis. This suggests that the mitotic cortex is poised close to a tension maximum. Finally, using a computational model, we identify a physical mechanism by which maximum tension is achieved at intermediate actin filament lengths. Our results indicate that actin network architecture, alongside myosin activity, is key to cell surface tension regulation. |
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