Abstract:
:Tight-junction-regulated actomyosin activity determines epithelial and endothelial tension on adherens junctions and drives morphogenetic processes; however, whether or not tight junctions themselves are under tensile stress is not clear. Here, we use a tension sensor based on ZO-1, a scaffolding protein that links the junctional membrane to the cytoskeleton, to determine if tight junctions carry a mechanical load. Our data indicate that ZO-1 is under mechanical tension and that forces acting on ZO-1 are regulated by extracellular matrix (ECM) stiffness and the junctional adhesion molecule JAM-A. JAM-A depletion stimulates junctional recruitment of p114RhoGEF/ARHGEF18, mechanical tension on ZO-1, and traction forces at focal adhesions. p114RhoGEF is required for activation of junctional actomyosin activity and tight junction integrity on stiff but not soft ECM. Thus, junctional ZO-1 bears a mechanical load, and junction assembly is regulated by interplay between the physical properties of the ECM and adhesion-regulated signaling at tight junctions.
journal_name
Cell Repjournal_title
Cell reportsauthors
Haas AJ,Zihni C,Ruppel A,Hartmann C,Ebnet K,Tada M,Balda MS,Matter Kdoi
10.1016/j.celrep.2020.107924subject
Has Abstractpub_date
2020-07-21 00:00:00pages
107924issue
3issn
2211-1247pii
S2211-1247(20)30905-0journal_volume
32pub_type
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