How tropomyosin regulates lamellipodial actin-based motility: A combined biochemical and reconstituted motility approach

Beáta Bugyi, Dominique Didry, Marie France Carlier

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

At the leading edge of migrating cells, protrusive forces are developed by the assembly of actin filaments organised in a lamellipodial dendritic array at the front and a more distal lamellar linear array. Whether these two arrays are distinct or functionally linked and how they contribute to cell migration is an open issue. Tropomyosin severely inhibits lamellipodium formation and facilitates the lamellar array while enhancing migration, by a mechanism that is not understood. Here we show that the complex in vivo effects of tropomyosin are recapitulated in the reconstituted propulsion of neural Wiskott-Aldrich syndrome protein (N-WASP)-functionalised beads, which is based on the sole formation of a dendritic array of actin-related protein (Arp)2/3-branched filaments. Actin-depolymerising factor (ADF) and tropomyosin control the length of the actin tail. By competing with Arp2/3 during filament branching, tropomyosin displays opposite effects on propulsion depending on the surface density of N-WASP. Tropomyosin binding to the dendritic array is facilitated following filament debranching, causing its enrichment at the rear of the actin tail, like in vivo. These results unveil the mechanism by which tropomyosin generates two morphologically and dynamically segregated actin networks from a single one.

Original languageEnglish
Pages (from-to)14-26
Number of pages13
JournalEMBO Journal
Volume29
Issue number1
DOIs
Publication statusPublished - Jan 6 2010

Keywords

  • Actin
  • Lamella
  • Lamellipodium
  • Protrusion
  • Reconstituted motility
  • Tropomyosin

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

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