Actin cortex architecture regulates cell surface tension

Nat Cell Biol. 2017 Jun;19(6):689-697. doi: 10.1038/ncb3525. Epub 2017 May 22.

Abstract

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.

Publication types

  • Video-Audio Media

MeSH terms

  • Actin Cytoskeleton / metabolism*
  • Actin Cytoskeleton / ultrastructure
  • Actins / metabolism*
  • Adaptor Proteins, Signal Transducing / genetics
  • Adaptor Proteins, Signal Transducing / metabolism
  • CapZ Actin Capping Protein / genetics
  • CapZ Actin Capping Protein / metabolism
  • Cell Cycle*
  • Cell Shape*
  • Cofilin 1 / genetics
  • Cofilin 1 / metabolism
  • Computer Simulation
  • Formins
  • HeLa Cells
  • Humans
  • Interphase
  • Mechanotransduction, Cellular*
  • Mitosis
  • Models, Biological
  • Surface Tension
  • Transfection

Substances

  • Actins
  • Adaptor Proteins, Signal Transducing
  • CAPZB protein, human
  • CFL1 protein, human
  • CapZ Actin Capping Protein
  • Cofilin 1
  • DIAPH1 protein, human
  • Formins