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Integrins stimulate E-cadherin-mediated intercellular adhesion by regulating Src-kinase activation and actomyosin
Clara Martinez-Rico1, Frederic Pincet, Jean-Paul Thiery
1UMR144 CNRS-Institut Curie, 75248 Paris Cedex 05, France.
Journal of Cell Science
|February 11, 2010
Summary
Integrins and cadherins, key cell adhesion molecules, communicate to control cell movement. This study reveals how integrin signals strengthen cadherin-based cell-cell adhesion through specific molecular pathways.
Area of Science:
- Cell Biology
- Biochemistry
- Molecular Biology
Background:
- Cadherins and integrins are critical adhesion molecules mediating cell-cell and cell-matrix interactions, respectively.
- Existing research suggests crosstalk between integrins and cadherins influences cell adhesion and motility.
Purpose of the Study:
- To investigate the role of integrins in modulating the strength of cadherin-mediated intercellular adhesion.
- To elucidate the molecular mechanisms underlying the crosstalk between integrins and cadherins.
Main Methods:
- Utilized a dual pipette assay to quantify the force required for separating cell doublets.
- Investigated the impact of fibronectin and vitronectin (ligands for integrins) on cell adhesion strength.
- Examined the involvement of specific signaling pathways, including ROCK, MLCK, and Src family kinases.
Main Results:
- Intercellular adhesion strength was significantly enhanced when cell doublets were adhered to fibronectin or vitronectin compared to polylysine.
- This integrin-mediated enhancement of adhesion was dependent on cell spreading and stimulation duration.
- Cadherin-7 expressing cells also showed increased adhesion upon fibronectin stimulation.
- Both cadherin-mediated adhesion establishment and integrin-regulated adhesion strength required ROCK, MLCK, and actomyosin contractility, with integrin signaling additionally needing Src family kinases.
Conclusions:
- Integrin stimulation strengthens cadherin-mediated cell-cell adhesion through activation of actomyosin contractility and Src family kinases.
- This molecular crosstalk between integrins and cadherins is crucial for regulating cell plasticity during tissue development (histogenesis) and shape formation (morphogenesis).
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01:17Intracellular Signaling Affects Focal Adhesions
Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
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01:10Integrins
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01:24Adherens Junctions
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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01:15Activation of Integrins
Integrins bind ligands and transmit information from outside the cell to inside or vice-versa through an "outside-in signaling" or "inside-out signaling."
In "outside-in signaling," external factors in the extracellular space bind to exposed ligand binding sites on integrins. This causes the inactive protein to undergo a conformational change to become active. Integrins are often clustered on the cell membrane. Repetitive and regularly spaced ligand binding events provide an effective stimulus.
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01:26Tension Response at Adherens Junctions
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01:03Anchoring Junctions
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