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Ena orchestrates remodelling within the actin cytoskeleton to drive robust Drosophila macrophage chemotaxis

Research output: Contribution to journalArticle

  • Andrew J. Davidson
  • Tom H. Millard
  • Iwan R. Evans
  • Will Wood
Original languageEnglish
Article numberjcs224618
Number of pages8
JournalJournal of Cell Science
Issue number5
Early online date4 Feb 2019
DateAccepted/In press - 15 Jan 2019
DateE-pub ahead of print - 4 Feb 2019
DatePublished (current) - 18 Feb 2019


The actin cytoskeleton is the engine that powers the inflammatory chemotaxis of immune cells to sites of tissue damage or infection. Here, we combine genetics with live in vivo imaging to investigate how cytoskeletal rearrangements drive macrophage recruitment to wounds in Drosophila. We find that the actin-regulatory protein Ena is a master regulator of lamellipodial dynamics in migrating macrophages, where it remodels the cytoskeleton to form linear filaments that can then be bundled together by the cross-linker Fascin (also known as Singed in flies). In contrast, the formin Dia generates rare, probing filopods for specialised functions that are not required for migration. The role of Ena in lamellipodial bundling is so fundamental that its overexpression increases bundling even in the absence of Fascin by marshalling the remaining cross-linking proteins to compensate. This reorganisation of the lamellipod generates cytoskeletal struts that push against the membrane to drive leading edge advancement and boost cell speed. Thus, Ena-mediated remodelling extracts the most from the cytoskeleton to power robust macrophage chemotaxis during their inflammatory recruitment to wounds.

    Research areas

  • Actin, Drosophila, Ena, Hemocyte, Macrophage, Migration

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    Rights statement: This is the final published version of the article (version of record). It first appeared online via The Company of Biologists at DOI: 10.1242/jcs.224618. Please refer to any applicable terms of use of the publisher.

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    Licence: CC BY


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