Junctional actin assembly is mediated by Formin-like 2 downstream of Rac1
| Autor: | Katharina Grikscheit, Ying Wang, Tanja Frank, Robert Grosse |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
rac1 GTP-Binding Protein
Cell signaling Arp2/3 complex Formins RAC1 macromolecular substances Cell Communication Biology Adherens junction Actin remodeling of neurons Report Humans Actin Research Articles Epithelial polarity fungi Proteins Epithelial Cells Cell Biology Adherens Junctions Actins Cell biology HEK293 Cells biology.protein Female HeLa Cells |
| Zdroj: | The Journal of Cell Biology |
| ISSN: | 1540-8140 0021-9525 |
| Popis: | Rac1 promotes the rapid and dynamic localization of Formin-like 2 (FMNL2) to adherens junctions, where it promotes actin assembly. Epithelial integrity is vitally important, and its deregulation causes early stage cancer. De novo formation of an adherens junction (AJ) between single epithelial cells requires coordinated, spatial actin dynamics, but the mechanisms steering nascent actin polymerization for cell–cell adhesion initiation are not well understood. Here we investigated real-time actin assembly during daughter cell–cell adhesion formation in human breast epithelial cells in 3D environments. We identify formin-like 2 (FMNL2) as being specifically required for actin assembly and turnover at newly formed cell–cell contacts as well as for human epithelial lumen formation. FMNL2 associates with components of the AJ complex involving Rac1 activity and the FMNL2 C terminus. Optogenetic control of Rac1 in living cells rapidly drove FMNL2 to epithelial cell–cell contact zones. Furthermore, Rac1-induced actin assembly and subsequent AJ formation critically depends on FMNL2. These data uncover FMNL2 as a driver for human epithelial AJ formation downstream of Rac1. |
| Databáze: | OpenAIRE |
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