Opposing roles for distinct LINC complexes in regulation of the small GTPase RhoA.
Autor: | Thakar K; Department of Cell Biology, Yale School of Medicine, New Haven, CT 06520., May CK; Department of Cell Biology, Yale School of Medicine, New Haven, CT 06520., Rogers A; Department of Cell Biology, Yale School of Medicine, New Haven, CT 06520., Carroll CW; Department of Cell Biology, Yale School of Medicine, New Haven, CT 06520 topher.carroll@yale.edu. |
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Jazyk: | angličtina |
Zdroj: | Molecular biology of the cell [Mol Biol Cell] 2017 Jan 01; Vol. 28 (1), pp. 182-191. Date of Electronic Publication: 2016 Nov 09. |
DOI: | 10.1091/mbc.E16-06-0467 |
Abstrakt: | Linker of Nucleoskeleton and Cytoskeleton (LINC) complexes span the nuclear envelope and transduce force from dynamic cytoskeletal networks to the nuclear lamina. Here we show that LINC complexes also signal from the nuclear envelope to critical regulators of the actin cytoskeleton. Specifically, we find that LINC complexes that contain the inner nuclear membrane protein Sun2 promote focal adhesion assembly by activating the small GTPase RhoA. A key effector in this process is the transcription factor/coactivator complex composed of SRF/Mkl1. A constitutively active form of SRF/Mkl1 was not sufficient to induce focal adhesion assembly in cells lacking Sun2, however, suggesting that LINC complexes support RhoA activity through a transcription-independent mechanism. Strikingly, we also find that the inner nuclear membrane protein Sun1 antagonizes Sun2 LINC complexes and inhibits RhoA activation and focal adhesion assembly. Thus different LINC complexes have opposing roles in the transcription-independent control of the actin cytoskeleton through the small GTPase RhoA. (© 2017 Thakar et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License(http://creativecommons.org/licenses/by-nc-sa/3.0).) |
Databáze: | MEDLINE |
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