PT  - JOURNAL ARTICLE
AU  - Eric T. Hall
AU  - Elizabeth Hoesing
AU  - Endre Sinkovics
AU  - Esther M. Verheyen
TI  - Actomyosin contractility modulates Wnt signaling through adherens junction stability
AID  - 10.1101/220178
DP  - 2017 Jan 01
TA  - bioRxiv
PG  - 220178
4099  - http://biorxiv.org/content/early/2017/11/15/220178.short
4100  - http://biorxiv.org/content/early/2017/11/15/220178.full
AB  - Mechanical forces can influence the canonical Wnt signaling pathway in processes like mesoderm differentiation and tissue stiffness during tumorigenesis, but a molecular mechanism involving both in a developing epithelium and its homeostasis is lacking. We identified that increased non-muscle myosin II activation and cellular contraction inhibited Wnt target gene transcription in developing Drosophila. Genetic interactions studies identified this effect was due to myosin-induced accumulation of cortical F-actin resulting in clustering and accumulation of E-cadherin to the adherens junctions. E-cadherin titrates any available β-catenin, the Wnt pathway transcriptional co-activator, to the adherens junctions in order to maintain cell-cell adhesion under contraction. We show that decreased levels of cytoplasmic β-catenin result in insufficient nuclear translocation for full Wnt target gene transcription. Our work elucidates a mechanism in which the dynamic activation of actomyosin contractility refines patterning of Wnt transcription during development and maintenance of epithelial tissue in organisms.