Yashar Bashirzadeh
(Department of Mechanical Engineering, University of Michigan, Ann Arbor, MI 48109, USA)
Hossein Moghimianavval
(Department of Mechanical Engineering, University of Michigan, Ann Arbor, MI 48109, USA)
Allen P. Liu
(Department of Mechanical Engineering, University of Michigan, Ann Arbor, MI 48109, USA; Department of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109, USA; Cellular and Molecular Biology Program, University of Michigan, Ann Arbor, MI 48109, USA; Department of Biophysics, University of Michigan, Ann Arbor, MI 48109, USA; Corresponding author)
Journal: iScience
•
• Elsevier
• ISSN: 2589-0042
Abstract
Summary: Cell shape changes from locomotion to cytokinesis are, to a large extent, driven by myosin-driven remodeling of cortical actin patterns. Passive crosslinkers such as α-actinin and fascin as well as actin nucleator Arp2/3 complex largely determine actin network architecture and, consequently, membrane shape changes. Here we reconstitute actomyosin networks inside cell-sized lipid bilayer vesicles and show that depending on vesicle size and concentrations of α-actinin and fascin actomyosin networks assemble into ring and aster-like patterns. Anchoring actin to the membrane does not change actin network architecture yet exerts forces and deforms the membrane when assembled in the form of a contractile ring. In the presence of α-actinin and fascin, an Arp2/3 complex-mediated actomyosin cortex is shown to assemble a ring-like pattern at the equatorial cortex followed by myosin-driven clustering and consequently blebbing. An active gel theory unifies a model for the observed membrane shape changes induced by the contractile cortex.