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Published on: March 8, 2017
Mechanosensitive EPLIN-dependent remodeling of adherens junctions regulates epithelial reshaping
Katsutoshi Taguchi1, Takashi Ishiuchi, Masatoshi Takeichi
1RIKEN Center for Developmental Biology, Minatojima-Minamimachi, Chuo-ku, Kobe 650-0047, Japan.
The Journal of Cell Biology
|August 17, 2011
Summary
Epithelial cells remodel adherens junctions (AJs) by converting zonula adherens (ZA) to punctate AJs (pAJs). EPLIN protein loss at pAJs suggests it acts as a mechanosensitive regulator of junctional architecture during cell reorganization.
Area of Science:
- Cell biology
- Biophysics
- Epithelial biology
Background:
- Adherens junctions (AJs), including the zonula adherens (ZA), are crucial for epithelial cell-cell adhesion.
- The mechanisms governing ZA remodeling during epithelial reorganization remain poorly understood.
Purpose of the Study:
- To investigate how epithelial cells remodel their junctional architecture during reorganization.
- To identify the molecular players and mechanical forces involved in ZA remodeling.
Main Methods:
- Microscopy to observe AJ morphology during epithelial colony formation.
- Biochemical assays to assess protein localization and interactions (EPLIN, αE-catenin, vinculin).
- Manipulation of actin cytoskeleton and junctional tension to study force-dependent regulation.
Main Results:
- ZA transforms into punctate AJs (pAJs) at epithelial colony margins.
- Epithelial protein lost in neoplasm (EPLIN), essential for ZA, is lost from pAJs.
- Junctional tension and lateral actin forces regulate EPLIN-AJ association.
- Vinculin and EPLIN cooperate to maintain ZA structure.
Conclusions:
- Epithelial cells dynamically remodel junctional architecture in response to mechanical cues.
- αE-catenin-bound EPLIN functions as a mechanosensitive regulator controlling ZA stability and pAJ formation.
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