bims-fascar Biomed News
on Phase separation and cellular architecture
Issue of 2019‒07‒21
two papers selected by
Victoria Yan
Max Planck Institute of Molecular Cell Biology and Genetics

  1. Biophys J. 2019 Jun 25. pii: S0006-3495(19)30507-7. [Epub ahead of print]
    Schramm AC, Hocky GM, Voth GA, Martiel JL, De La Cruz EM.
      The assembly of actin filaments and filament networks generate forces that drive cell and vesicle movement. These structures and the comprising actin filaments must be mechanically stable to sustain these forces and maintain their structural integrity. Filaments in these dynamic structures must also be disassembled to recycle and replenish the pool of actin monomers available for polymerization. Actin-severing proteins such as cofilin and contractile myosin motor proteins fragment these nominally stable structures. We developed a mesoscopic-length-scale actin filament model to investigate force-induced filament fragmentation. We show that fragmentation in our model occurs at curvatures similar to previous measurements of fragmentation within (cofil)actin and actin-cofilactin boundaries. Boundaries between bare and cofilin-decorated segments are brittle and fragment at small bending and twisting deformations. Extending filaments disperses strain uniformly over subunit interfaces, and filaments fragment with no detectable partial rupture or plastic deformation. In contrast, bending or twisting filaments imposes nonuniform interface strain and leads to partial interface rupture, accelerating filament fragmentation. As a result, the rupture force under compressive loads is an order of magnitude lower than under tensile loads. Partial interface rupture may be a primary mechanism of accelerating actin filament fragmentation by other actin-destabilizing proteins.
  2. Phys Rev Lett. 2019 Jun 21. 122(24): 248102
    Liu G, Patch A, Bahar F, Yllanes D, Welch RD, Marchetti MC, Thutupalli S, Shaevitz JW.
      Combining high-resolution single cell tracking experiments with numerical simulations, we show that starvation-induced fruiting body formation in Myxococcus xanthus is a phase separation driven by cells that tune their motility over time. The phase separation can be understood in terms of cell density and a dimensionless Péclet number that captures cell motility through speed and reversal frequency. Our work suggests that M. xanthus takes advantage of a self-driven nonequilibrium phase transition that can be controlled at the single cell level.