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The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
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The cadherins were one of the first cell adhesion molecules discovered; the term “cadherins”   is based on their calcium-dependent adhering properties. The first cadherins discovered on the epithelial, neuronal, and placental cells were named E-cadherin, P-cadherin, and N-cadherin, respectively. These classical cadherins share sequence and structural similarities. Other cadherins, including those involved in cell signaling, are grouped into non-classical cadherins. This...
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In animal cells, the extracellular matrix allows cells within tissues to withstand external stresses and transmits signals from the outside of the cell to the inside. The extracellular matrix is extensive, and its composition varies between different types of tissues. For example, the reticular fibers and ground substance make up the ECM in loose connective tissue, while collagen and bone minerals make up the ECM of bone tissue. 
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Strong contact points between adjacent cells anchor them to each other, forming tissues. Such anchoring junctions are of two types –  adherens junctions and desmosomes. Adherens junctions are abundant in tissues such as  epithelium and endothelium, forming a continuous zone of adhesion called the adhesion belt. In other tissues, such as  heart muscle, they appear as clusters, linking the cells to produce coordinated heart muscle contraction.
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Catenins are characterized by multiple binding domains and dynamic structures that allow them to function as linker proteins in cell junction complexes. All catenins, except α-catenin, contain a characteristic protein sequence called the armadillo repeat and are therefore also called armadillo proteins.
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Bead Aggregation Assays for the Characterization of Putative Cell Adhesion Molecules
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Changes in E-cadherin rigidity sensing regulate cell adhesion.

Caitlin Collins1, Aleksandra K Denisin2,3, Beth L Pruitt2,3

  • 1Department of Biology, Stanford University, Stanford, CA 94305.

Proceedings of the National Academy of Sciences of the United States of America
|July 5, 2017
PubMed
Summary
This summary is machine-generated.

Epithelial cells sense substrate stiffness through E-cadherin, altering cell shape and actin dynamics. This mechanical sensing regulates cell-cell adhesion initiation by controlling actin-based protrusions.

Keywords:
Cdc42E-cadherinactin dynamicsforminsrigidity

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Area of Science:

  • Cell biology
  • Biophysics
  • Mechanobiology

Background:

  • Cell adhesion complexes transduce mechanical cues to regulate cell behavior.
  • Integrin-mediated extracellular matrix rigidity sensing is well-studied.
  • Cadherin-mediated rigidity sensing during cell adhesion is largely unexplored.

Purpose of the Study:

  • To investigate E-cadherin-mediated rigidity sensing during epithelial cell adhesion.
  • To explore the role of mechanical cues in regulating cell morphology, actin organization, and membrane dynamics via E-cadherin.

Main Methods:

  • Mechanically tunable polyacrylamide (PA) gels functionalized with E-cadherin (Ecad-Fc).
  • Traction force microscopy (TFM) to analyze cellular tractions and actin organization.
  • Quantitative 3D cell-cell adhesion assays and live cell imaging.

Main Results:

  • E-cadherin-dependent cell adhesion was sensitive to substrate stiffness (PA gel elastic modulus).
  • Cells reorganized traction-stress regions and actin-based protrusions (filopodia/lamellipodia) in response to substrate rigidity.
  • Cdc42, formin, and Arp2/3 signaling pathways were differentially required for adhesion initiation based on stiffness.

Conclusions:

  • E-cadherin rigidity sensing influences cell morphology, actin organization, and membrane dynamics.
  • Signaling molecules activated by E-cadherin rigidity sensing contribute to actin organization and membrane dynamics during cell-cell adhesion initiation.
  • A transition in E-cadherin interaction stiffness may regulate actin and membrane dynamics during initial cell-cell adhesion.