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Dev Cell. 2015 Jan 12;32(1):43-53. doi: 10.1016/j.devcel.2014.10.027. Epub 2014 Dec 24.

Profilin regulates F-actin network homeostasis by favoring formin over Arp2/3 complex.

Author information

1
Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, IL 60637, USA.
2
Department of Cell and Developmental Biology, State University of New York (SUNY) Upstate Medical University, 750 East Adams Street, Syracuse, NY 13210, USA.
3
Department of Cell and Developmental Biology, State University of New York (SUNY) Upstate Medical University, 750 East Adams Street, Syracuse, NY 13210, USA. Electronic address: sirotkiv@upstate.edu.
4
Department 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. Electronic address: drkovar@uchicago.edu.

Abstract

Fission yeast cells use Arp2/3 complex and formin to assemble diverse filamentous actin (F-actin) networks within a common cytoplasm for endocytosis, division, and polarization. Although these homeostatic F-actin networks are usually investigated separately, competition for a limited pool of actin monomers (G-actin) helps to regulate their size and density. However, the mechanism by which G-actin is correctly distributed between rival F-actin networks is not clear. Using a combination of cell biological approaches and in vitro reconstitution of competition between actin assembly factors, we found that the small G-actin binding protein profilin directly inhibits Arp2/3 complex-mediated actin assembly. Profilin is therefore required for formin to compete effectively with excess Arp2/3 complex for limited G-actin and to assemble F-actin for contractile ring formation in dividing cells.

PMID:
25543282
PMCID:
PMC4293355
DOI:
10.1016/j.devcel.2014.10.027
[Indexed for MEDLINE]
Free PMC Article

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