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Related Concept Videos

Adherens Junctions01:24

Adherens Junctions

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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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Structure of Cadherins01:25

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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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Tension Response at Adherens Junctions01:26

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The adherens junctions that anchor cells together are multi-protein complexes that dynamically adapt to mechanical stimuli such as tensile forces and shear stress. Mechanosensory proteins in these junctions can sense such mechanical stimuli and undergo a shift in their conformation, resulting in an altered function — a process called mechanotransduction.
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Catenins01:23

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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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Cadherins in Tissue Organization01:19

Cadherins in Tissue Organization

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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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Mechanism of Lamellipodia Formation01:31

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Cells migrating in response to external stimuli form lamellipodia, which are thin membrane protrusions supported by a mesh of linked, branched, or unbranched actin filaments. These actin filaments interact with myosin motor proteins, creating the dynamic actomyosin complex within the cytoskeleton. Contractility, or the ability to generate contractile stress, is inherent to the actomyosin complex. It helps cells detect the stiffness of the surrounding ECM and exert contractile force for...
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Forming, Confining, and Observing Microtubule-Based Active Nematics
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E-cadherin junction formation involves an active kinetic nucleation process.

Kabir H Biswas1, Kevin L Hartman2, Cheng-han Yu1

  • 1Mechanobiology Institute, National University of Singapore, Singapore 117411;

Proceedings of the National Academy of Sciences of the United States of America
|August 21, 2015
PubMed
Summary
This summary is machine-generated.

Researchers reconstituted epithelial (E)-cadherin junctions using live cells and supported membranes. This revealed that cell activity and low E-cadherin extracellular domain mobility are crucial for forming these hybrid junctions.

Keywords:
adhesionbilayercadherindiffusionnucleation

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Area of Science:

  • Cell biology
  • Biophysics
  • Biochemistry

Background:

  • Epithelial (E)-cadherin mediated cell-cell junctions are vital for tissue structure and mechanical/biochemical signaling.
  • Understanding E-cadherin adhesion mechanisms is key to tissue development and disease research.

Purpose of the Study:

  • To reconstitute and analyze junction-like structures formed between native E-cadherin in living cells and the extracellular domain of E-cadherin (E-cad-ECD) in a supported membrane.
  • To investigate the requirements and initial stages of hybrid junction formation.

Main Methods:

  • In vitro reconstitution of hybrid live cell-supported membrane systems.
  • Utilizing native E-cadherin in living cells and E-cad-ECD in a supported membrane with controlled mobility.
  • Observing junction formation, recruitment of α-catenin, and cortical actin remodeling.

Main Results:

  • Successful in vitro reconstitution of junction-like structures between live cells and supported membranes.
  • Junction formation requires active cellular processes and low mobility of E-cad-ECD in the supported membrane.
  • Hybrid junctions recruit α-catenin and induce cortical actin remodeling.
  • Initial junction formation depends on trans E-cadherin interactions and involves filopodia dynamics.

Conclusions:

  • The study successfully established a novel hybrid system for studying E-cadherin-mediated cell-cell junctions in vitro.
  • Active cellular processes and specific E-cadherin interactions (trans, not cis) are essential for initiating junction formation.
  • Filopodia dynamics play a critical role in the nucleation of these hybrid junctions.