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WASP family proteins and formins compete in pseudopod- and bleb-based migration

Research output: Contribution to journalArticle

  • Andrew J. Davidson
  • Clelia Amato
  • Peter A. Thomason
  • Robert H. Insall
Original languageEnglish
Pages (from-to)701-714
Number of pages14
JournalJournal of Cell Biology
Volume217
Issue number2
DOIs
DateAccepted/In press - 6 Nov 2017
DatePublished (current) - 1 Feb 2018

Abstract

Actin pseudopods induced by SCAR/WAVE drive normal migration and chemotaxis in eukaryotic cells. Cells can also migrate using blebs, in which the edge is driven forward by hydrostatic pressure instead of actin. In Dictyostelium discoideum, loss of SCAR is compensated by WASP moving to the leading edge to generate morphologically normal pseudopods. Here we use an inducible double knockout to show that cells lacking both SCAR and WASP are unable to grow, make pseudopods or, unexpectedly, migrate using blebs. Remarkably, amounts and dynamics of actin polymerization are normal. Pseudopods are replaced in double SCAR/WASP mutants by aberrant filopods, induced by the formin dDia2. Further disruption of the gene for dDia2 restores cells' ability to initiate blebs and thus migrate, though pseudopods are still lost. Triple knockout cells still contain near-normal F-actin levels. This work shows that SCAR, WASP, and dDia2 compete for actin. Loss of SCAR and WASP causes excessive dDia2 activity, maintaining F-actin levels but blocking pseudopod and bleb formation and migration.

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    Rights statement: This is the final published version of the article (version of record). It first appeared online via Rockefeller University Press at https://doi.org/10.1083/jcb.201705160 . Please refer to any applicable terms of use of the publisher.

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