期刊
NATURE CELL BIOLOGY
卷 19, 期 6, 页码 689-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncb3525
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资金
- Medical Research Council UK (MRC) [MC_UU_12018/5]
- Human Frontier Science Program
- European Research Council [311637-MorphoCorDiv]
- Polish Ministry of Science and Higher Education [454/N-MPG/2009/0]
- Canadian Institutes of Health Research (CIHR) [MOP123408]
- Spanish Ministry of Economy and Competitiveness [BFU2010-16546]
- Centro de Excelencia Severo Ochoa [SEV-2012-0208]
- CERCA Programme/Generalitat de Catalunya
- Fonds de Recherche Sante Quebec (FRQS)
- Francis Crick Institute
- Cancer Research UK [FC001317]
- UK Medical Research Council [FC001317]
- Wellcome Trust [FC001317]
- MRC [MC_UP_1205/1, MC_UU_00012/5, MC_UU_12018/5] Funding Source: UKRI
- Cancer Research UK [21144] Funding Source: researchfish
- Medical Research Council [MC_UP_1205/1, MC_UU_00012/5, MC_UU_12018/5] Funding Source: researchfish
- MRC Laboratory for Molecular Cell Biology (LMCB) [HFSP Research Grant, Paluch ERC Research Grant] Funding Source: researchfish
- The Francis Crick Institute [10317] Funding Source: researchfish
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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