Pak1 and PP2A antagonize aPKC function to support cortical tension induced by the Crumbs-Yurt complex
Cornelia Biehler,
Katheryn E Rothenberg,
Alexandra Jette,
Helori-Mael Gaude,
Rodrigo Fernandez-Gonzalez,
Patrick Laprise
Affiliations
Cornelia Biehler
Centre de Recherche sur le Cancer, Université Laval, Québec, Canada; axe oncologie du Centre de Recherche du Centre Hospitalier Universitaire de Québec-UL, Québec, Canada
Institute of Biomedical Engineering, University of Toronto, Toronto, Canada; Ted Rogers Centre for Heart Research, University of Toronto, Toronto, Canada
Centre de Recherche sur le Cancer, Université Laval, Québec, Canada; axe oncologie du Centre de Recherche du Centre Hospitalier Universitaire de Québec-UL, Québec, Canada
Helori-Mael Gaude
Centre de Recherche sur le Cancer, Université Laval, Québec, Canada; axe oncologie du Centre de Recherche du Centre Hospitalier Universitaire de Québec-UL, Québec, Canada
Institute of Biomedical Engineering, University of Toronto, Toronto, Canada; Ted Rogers Centre for Heart Research, University of Toronto, Toronto, Canada; Department of Cell and Systems Biology, University of Toronto, Toronto, Canada; Developmental and Stem Cell Biology Program, The Hospital for Sick Children, Toronto, Canada
Centre de Recherche sur le Cancer, Université Laval, Québec, Canada; axe oncologie du Centre de Recherche du Centre Hospitalier Universitaire de Québec-UL, Québec, Canada
The Drosophila polarity protein Crumbs is essential for the establishment and growth of the apical domain in epithelial cells. The protein Yurt limits the ability of Crumbs to promote apical membrane growth, thereby defining proper apical/lateral membrane ratio that is crucial for forming and maintaining complex epithelial structures such as tubes or acini. Here, we show that Yurt also increases Myosin-dependent cortical tension downstream of Crumbs. Yurt overexpression thus induces apical constriction in epithelial cells. The kinase aPKC phosphorylates Yurt, thereby dislodging the latter from the apical domain and releasing apical tension. In contrast, the kinase Pak1 promotes Yurt dephosphorylation through activation of the phosphatase PP2A. The Pak1–PP2A module thus opposes aPKC function and supports Yurt-induced apical constriction. Hence, the complex interplay between Yurt, aPKC, Pak1, and PP2A contributes to the functional plasticity of Crumbs. Overall, our data increase our understanding of how proteins sustaining epithelial cell polarization and Myosin-dependent cell contractility interact with one another to control epithelial tissue architecture.