Arrestins regulate cell spreading and motility via focal adhesion dynamics
| Autor: | Whitney M. Cleghorn, Irina Kaverina, Eugenia V. Gurevich, Nada Bulus, Vsevolod V. Gurevich, Kevin M. Branch, Christopher Arnette, Alissa M. Weaver, Seunghyi Kook, Roy Zent |
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| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
genetic structures
Arrestins Motility Clathrin binding Biology Clathrin Focal adhesion 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Microtubule Cell Movement Arrestin Cell Adhesion Animals Cell adhesion Molecular Biology 030304 developmental biology 0303 health sciences Focal Adhesions Cell Biology Articles Fibroblasts eye diseases Cell biology Nocodazole Cell Motility chemistry biology.protein sense organs 030217 neurology & neurosurgery |
| Zdroj: | Molecular Biology of the Cell |
| ISSN: | 1939-4586 1059-1524 |
| Popis: | Cells lacking both nonvisual arrestins show excessive spreading, defects in focal adhesion disassembly, and sensitivity to microtubules. This phenotype is rescued by wild-type arrestins but not mutants deficient in clathrin binding, suggesting that arrestins regulate focal adhesion disassembly by linking microtubules and clathrin. Focal adhesions (FAs) play a key role in cell attachment, and their timely disassembly is required for cell motility. Both microtubule-dependent targeting and recruitment of clathrin are critical for FA disassembly. Here we identify nonvisual arrestins as molecular links between microtubules and clathrin. Cells lacking both nonvisual arrestins showed excessive spreading on fibronectin and poly-d-lysine, increased adhesion, and reduced motility. The absence of arrestins greatly increases the size and lifespan of FAs, indicating that arrestins are necessary for rapid FA turnover. In nocodazole washout assays, FAs in arrestin-deficient cells were unresponsive to disassociation or regrowth of microtubules, suggesting that arrestins are necessary for microtubule targeting–dependent FA disassembly. Clathrin exhibited decreased dynamics near FA in arrestin-deficient cells. In contrast to wild-type arrestins, mutants deficient in clathrin binding did not rescue the phenotype. Collectively the data indicate that arrestins are key regulators of FA disassembly linking microtubules and clathrin. |
| Databáze: | OpenAIRE |
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