2. Academic Validation
  3. Oxidation of F-actin controls the terminal steps of cytokinesis

Oxidation of F-actin controls the terminal steps of cytokinesis

  • Nat Commun. 2017 Feb 23;8:14528. doi: 10.1038/ncomms14528.
Stéphane Frémont 1 2,  Hussein Hammich 3,  Jian Bai 1 2 4,  Hugo Wioland 5,  Kerstin Klinkert 1 2 4,  Murielle Rocancourt 1 2,  Carlos Kikuti 3,  David Stroebel 6,  Guillaume Romet-Lemonne 5,  Olena Pylypenko 3,  Anne Houdusse 3,  Arnaud Echard 1 2
Affiliations

Affiliations

  • 1 Membrane Traffic and Cell Division Lab, Cell Biology and Infection Department Institut Pasteur, 25-28 rue du Dr Roux, 75724 Paris Cedex 15, France.
  • 2 Centre National de la Recherche Scientifique UMR3691, 75015 Paris, France.
  • 3 Structural Motility, Institut Curie, PSL Research University, CNRS, UMR 144, F-75005 Paris, France.
  • 4 Sorbonne Universités, UPMC Univ Paris06, Sorbonne Universités, IFD, 4 Place Jussieu, 75252 Paris Cedex 15, France.
  • 5 Institut Jacques Monod, CNRS, Université Paris Diderot, Université Sorbonne Paris Cité, 75013 Paris, France.
  • 6 Ecole Normale Supérieure, PSL Research University, CNRS, INSERM, Institut de Biologie de l'École Normale Supérieure (IBENS), 75005 Paris, France.
PMID: 28230050 DOI: 10.1038/ncomms14528
Abstract

Cytokinetic abscission, the terminal step of cell division, crucially depends on the local constriction of ESCRT-III helices after Cytoskeleton disassembly. While the microtubules of the intercellular bridge are cut by the ESCRT-associated Enzyme Spastin, the mechanism that clears F-actin at the abscission site is unknown. Here we show that oxidation-mediated depolymerization of actin by the redox Enzyme MICAL1 is key for ESCRT-III recruitment and successful abscission. MICAL1 is recruited to the abscission site by the Rab35 GTPase through a direct interaction with a flat three-helix domain found in MICAL1 C terminus. Mechanistically, in vitro assays on single actin filaments demonstrate that MICAL1 is activated by Rab35. Moreover, in our experimental conditions, MICAL1 does not act as a severing Enzyme, as initially thought, but instead induces F-actin depolymerization from both ends. Our work reveals an unexpected role for oxidoreduction in triggering local actin depolymerization to control a fundamental step of cell division.

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