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Publication Detail
Actin depolymerization-based force retracts the cell rear in polarizing and migrating cells.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Mseka T, Cramer LP
  • Publication date:
  • Pagination:
    2085, 2091
  • Journal:
    Curr Biol
  • Volume:
  • Issue:
  • Status:
  • Country:
  • PII:
  • Language:
  • Keywords:
    Actin Cytoskeleton, Actins, Animals, Cell Movement, Cell Polarity, Chick Embryo, Fibroblasts, Heart, Myocardium, Myosin Type II
In migrating cells, the relative importance of myosin II contractility for cell rear retraction varies [1-12]. However, in myosin II-inhibited polarizing cells, actin organization is compromised [13-18]; thus it remains unclear whether myosin II is simply required for correct actin arrangement or also directly drives rear retraction [9]. Ascaris sperm cells lack actin and associated motors, and depolymerization of major sperm protein is instead thought to pull the cell rear forward [19, 20]. Opposing views exist on whether actin could also have this function [19, 20] and has not been directly experimentally sought. We probe function at high temporal resolution in polarizing fibroblasts that establish migration by forming the cell rear first [9, 15, 21]. We show that in cells with correctly organized actin, that actin filament depolymerization directly drives retraction of the rear margin to polarize cells and spatially accounts for most cell rear retraction during established migration. Myosin II contractility is required early, to form aligned actin bundles that are needed for polarization, and also later to maintain bundle length that ensures directed protrusion at the cell front. Our data imply a new mechanism: actin depolymerization-based force retracts the cell rear to polarize cells with no direct contribution from myosin II contractility.
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