Physical mechanisms of ESCRT-III–driven cell division

Abstract

Living systems propagate by undergoing rounds of cell growth and division. Cell division is at heart a physical process that requires mechanical forces, usually exerted by assemblies of cytoskeletal polymers. Here we developed a physical model for the ESCRT-III–mediated division of archaeal cells, which despite their structural simplicity share machinery and evolutionary origins with eukaryotes. By comparing the dynamics of simulations with data collected from live cell imaging experiments, we propose that this branch of life uses a previously unidentified division mechanism. Active changes in the curvature of elastic cytoskeletal filaments can lead to filament perversions and supercoiling, to drive ring constriction and deform the overlying membrane. Abscission is then completed following filament disassembly. The model was also used to explore how different adenosine triphosphate (ATP)-driven processes that govern the way the structure of the filament is changed likely impact the robustness and symmetry of the resulting division. Comparisons between midcell constriction dynamics in simulations and experiments reveal a good agreement with the process when changes in curvature are implemented at random positions along the filament, supporting this as a possible mechanism of ESCRT-III–dependent division in this system. Beyond archaea, this study pinpoints a general mechanism of cytokinesis based on dynamic coupling between a coiling filament and the membrane.

Investigating the entropic nature of membrane-mediated interactions driving the aggregation of peripheral proteins

“…Biomembranes are physical and chemical boundaries of cells and many of their organelles, as well as quasi-two-dimensional universes of encounters and actions responsible for a vast variety of vital functions. 1 Many aspects of membrane dynamics, configuration, topology, and even composition are actively controlled by membrane-associated proteins, facilitating, among others, cellular motility, 2 proliferation, 3 response to stimuli, 4 trafficking and endo/exocytosis. 5–9 This renders the understanding of localization, organization and action of these proteins of utmost importance.…”

Molecular mechanism of GTP binding- and dimerization-induced enhancement of Sar1-mediated membrane remodeling

“…Recently, atomistic and coarse-grained MD simulations were employed to elucidate the molecular mechanism of membrane invagination and cell division driven by the Endosomal Sorting Complex Required for Transport III (ESCRT-III). (21–23) Further, combined all-atom and continuum elastic model-based calculations indicated that spontaneous curvature of an inclusion varies non-monotonically with the inclusion height of the bound protein/peptide. (24) Nevertheless, to date, an understanding of how amino acid sequence and penetration of a membrane binding protein motif controls the membrane curvature generation process remains incomplete.…”

A Review of Mechanics-Based Mesoscopic Membrane Remodelling Methods: Capturing Both the Physics and the Chemical Diversity

“…Also, some of the early analytical papers written by Thomas Fischer [35][36][37][38][39] , Udo Seifert [40][41][42] and Reinhard Lipowsky [43][44][45] have set the stage for deeper theoretical and computational studies in large scale membrane deformation. Also, several numerical simulation methods such as dissipative particle dynamics (DPD), Brownian dynamics (BD) and molecular dynamics (MD) have been used to study protein-mediated membrane remodelling at mesoscopic scales 23, [27][28][29][46][47][48][49][50][51][52][53][54][55][56] . In this review, we do not discuss mesoscopic models for membrane remodeling where the lipids and proteins are represented as discrete particles and the the Hamiltonian (force-field) is solved with the evolution methods such as DPD, BD or MD.…”