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Dev Cell. 2014 Feb 24;28(4):394-408. doi: 10.1016/j.devcel.2014.01.015.

Enabled negatively regulates diaphanous-driven actin dynamics in vitro and in vivo.

Author information

  • 1Biology Department, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
  • 2Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, IL 60637, USA.
  • 3Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
  • 4Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY, UK.
  • 5Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, IL 60637, USA; Department of Biochemistry and Molecular Biology, The University of Chicago, Chicago, IL 60637, USA.
  • 6Biology Department, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. Electronic address: peifer@unc.edu.

Abstract

Actin regulators facilitate cell migration by controlling cell protrusion architecture and dynamics. As the behavior of individual actin regulators becomes clear, we must address why cells require multiple regulators with similar functions and how they cooperate to create diverse protrusions. We characterized Diaphanous (Dia) and Enabled (Ena) as a model, using complementary approaches: cell culture, biophysical analysis, and Drosophila morphogenesis. We found that Dia and Ena have distinct biochemical properties that contribute to the different protrusion morphologies each induces. Dia is a more processive, faster elongator, paralleling the long, stable filopodia it induces in vivo, while Ena promotes filopodia with more dynamic changes in number, length, and lifetime. Acting together, Ena and Dia induce protrusions distinct from those induced by either alone, with Ena reducing Dia-driven protrusion length and number. Consistent with this, EnaEVH1 binds Dia directly and inhibits DiaFH1FH2-mediated nucleation in vitro. Finally, Ena rescues hemocyte migration defects caused by activated Dia.

Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.

PMID:
24576424
[PubMed - indexed for MEDLINE]
PMCID:
PMC3992947
Free PMC Article
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