BABS2202 Chap.12 Cell–Cell and Cell–Matrix Adhesion
Cell–Cell and Cell–Matrix Adhesion
Adhesion is an active information system. Cell–cell junctions connect neighbouring cells to cytoskeletons, regulate tissue mechanics and create barriers or communication routes. Cell–matrix adhesions connect extracellular ligands through receptors to actin or other internal structures, while signalling complexes alter survival, migration, polarity and gene expression.
The extracellular matrix is not inert packing: its composition, organisation and stiffness provide biochemical and mechanical cues that cells remodel and interpret.
Different junctions perform different tasks. Barrier-forming contacts regulate movement between epithelial cells. Anchoring junctions distribute force through actin or intermediate filaments.
Communicating junctions permit selected small molecules or ions to pass directly between cells. Integrin-based adhesions bind matrix outside and connect to adaptors and cytoskeleton inside; affinity and clustering can be regulated from either side of the membrane. Mechanotransduction converts force or substrate properties into biochemical changes.
Experimental claims should separate attachment strength, spreading, migration, polarity, barrier function and survival. Reduced retained cells after washing might reflect defective binding, increased death or altered cell number before the assay, so normalisation and time-resolved imaging are essential.
What this chapter covers
- 01
Cell–cell recognition and adhesion receptors in tissue organisation
- 02
Barrier junctions, anchoring junctions and communicating junctions as distinct functional arrangements
- 03
Actin and intermediate-filament coupling as routes for force distribution
- 04
Integrin activation, clustering, extracellular ligand binding and intracellular adaptor assembly
- 05
Extracellular-matrix composition, architecture, remodelling and growth-factor presentation
- 06
Focal adhesions, traction, migration, polarity and mechanotransduction
- 07
Attachment, spreading, migration, barrier and force assays with appropriate normalisation
Diagnosing reduced cell retention on matrix
- +1Possible explanations include poor initial receptor binding, failure to strengthen adhesions after binding, or reduced viable cell input.
- +1Standardise viable cell number and measure very early attachment before extensive spreading or death occurs.
- +1Follow spreading, adhesion-complex assembly and detachment force or wash sensitivity through time.
- +1Restore the altered receptor or adaptor and compare several matrix ligands to test specificity and causality.
Key terms
- Cell junction
- An organised cell–cell contact containing selected adhesion, scaffold, cytoskeletal or communication components suited to a tissue function.
- Integrin
- A heterodimeric adhesion receptor that binds extracellular ligands and connects through adaptors to intracellular signalling and cytoskeletal systems.
- Focal adhesion
- A dynamic integrin-associated complex that links matrix, signalling proteins and actin while transmitting and sensing force.
- Extracellular matrix
- A secreted and organised network outside cells that provides structural, adhesive, biochemical and mechanical information.
- Mechanotransduction
- Conversion of mechanical force or material properties into biochemical and cellular responses.
- Polarity
- Asymmetric organisation of cellular structure and function along one or more axes, often coordinated with adhesion and tissue context.
Cell–Cell and Cell–Matrix Adhesion FAQ
Is the extracellular matrix only structural support?
No. It binds receptors, presents or stores signalling molecules, guides migration, resists and transmits force, and is continually remodelled. Matrix composition, geometry and stiffness can change cell survival, differentiation and gene expression.
Do stronger adhesions always improve migration?
No. Migration requires attachment at the front, force transmission and release at the rear. Too little adhesion prevents traction, while excessively stable adhesion can impede turnover. The relation depends on receptor, matrix, force and cell type.
How can I measure barrier function?
Use a readout of movement across a cell layer or an electrical property aligned with junction integrity, alongside imaging and cell-condition controls. Junction-protein abundance alone does not establish that contacts are continuous, correctly located or functionally restrictive.
Does co-localisation of two adhesion proteins prove interaction?
No. It shows proximity at the imaging resolution. Test dependence, biochemical or biophysical association and interaction-site mutants while controlling abundance and localisation. Proteins can occupy the same adhesion complex without directly contacting each other.
Exam move
Draw each junction as outside receptor, membrane, adaptor and cytoskeletal connection, then write its tissue-level job. Compare cell–cell and cell–matrix adhesions without assuming one receptor family performs every task. For experiments, split the phenotype into viable input, initial attachment, spreading, adhesion maturation, force, migration and barrier function.
Practise moving from a molecular defect to tissue consequence while naming the assay that supports each step. Add a force-direction arrow to each diagram and ask where that force is resisted or transmitted. Build a second table separating abundance, localisation and function: normal receptor abundance with poor surface localisation predicts something different from correct localisation with weak cytoskeletal coupling.
Rehearse an epithelial-barrier scenario and a migrating-cell scenario because the same molecule can contribute differently to stable tissue architecture and dynamic movement. In every case, state the matrix ligand or neighbouring cell type rather than treating adhesion as context-free stickiness.
Finally, compare a static image with live tracking and a functional barrier or force assay; each sees a different property, and their agreement supports the bridge from molecular organisation to tissue performance.
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