4.7 Article

Mechanosensitive EPLIN-dependent remodeling of adherens junctions regulates epithelial reshaping

Journal

JOURNAL OF CELL BIOLOGY
Volume 194, Issue 4, Pages 643-656

Publisher

ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201104124

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Funding

  1. Ministry of Education, Science, Sports, and Culture of Japan
  2. Grants-in-Aid for Scientific Research [20002009] Funding Source: KAKEN

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The zonula adherens (ZA), a type of adherens junction (AJ), plays a major role in epithelial cell-cell adhesions. It remains unknown how the ZA is remodeled during epithelial reorganization. Here we found that the ZA was converted to another type of AJ with punctate morphology (pAJ) at the margins of epithelial colonies. The F-actin-stabilizing protein EPLIN (epithelial protein lost in neoplasm), which functions to maintain the ZA via its association with. E-catenin, was lost in the pAJs. Consistently, a fusion of. E-catenin and EPLIN contributed to the formation of ZA but not pAJs. We show that junctional tension was important for retaining EPLIN at AJs, and another force derived from actin fibers laterally attached to the pAJs inhibited EPLIN-AJ association. Vinculin was required for general AJ formation, and it cooperated with EPLIN to maintain the ZA. These findings suggest that epithelial cells remodel their junctional architecture by responding to mechanical forces, and the. E-catenin-bound EPLIN acts as a mechanosensitive regulator for this process.

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