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The atypical Rho GTPase RhoD is a regulator of actin cytoskeleton dynamics and directed cell migration
Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet.
Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology. Uppsala University, Science for Life Laboratory, SciLifeLab.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology. Uppsala University, Science for Life Laboratory, SciLifeLab. (Kreuger)
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2017 (English)In: Experimental Cell Research, ISSN 0014-4827, E-ISSN 1090-2422, Vol. 352, no 2, 255-264 p.Article in journal (Refereed) Published
Abstract [en]

RhoD belongs to the Rho GTPases, a protein family responsible for the regulation and organization of the actin cytoskeleton, and, consequently, many cellular processes like cell migration, cell division and vesicle trafficking. Here, we demonstrate that the actin cytoskeleton is dynamically regulated by increased or decreased protein levels of RhoD. Ectopic expression of RhoD has previously been shown to give an intertwined weave of actin filaments. We show that this RhoD-dependent effect is detected in several cell types and results in a less dynamic actin filament system. In contrast, RhoD depletion leads to increased actin filament-containing structures, such as cortical actin, stress fibers and edge ruffles. Moreover, vital cellular functions such as cell migration and proliferation are defective when RhoD is silenced. Taken together, we present data suggesting that RhoD is an important component in the control of actin dynamics and directed cell migration.

Place, publisher, year, edition, pages
2017. Vol. 352, no 2, 255-264 p.
Keyword [en]
RhoD, Rho GTPase, Actin, Stress fiber, Cell migration
National Category
Cell and Molecular Biology
Research subject
Medical Cell Biology
Identifiers
URN: urn:nbn:se:uu:diva-319045DOI: 10.1016/j.yexcr.2017.02.013ISI: 000396964600010PubMedID: 28196728OAI: oai:DiVA.org:uu-319045DiVA: diva2:1085937
Funder
The Karolinska Institutet's Research FoundationSwedish Cancer Society, JK-2014/820 PA-2014/0644
Available from: 2017-03-30 Created: 2017-03-30 Last updated: 2017-04-18Bibliographically approved

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