Contact signalling and cell motility.
There is now clear evidence that signals can be generated when cells make adhesions. This happens when contacts are made with the extracellular matrix, with other cells or with experimental substrata. It is shown that intracellular signals are triggered in a variety of situations by the aggregation of transmembrane glycoproteins. Such aggregation occurs at adhesion sites, and it is suggested that adhesion molecules which are capable of lateral diffusion become trapped at developing adhesion sites because their headgroups bind to arrays of external ligands. Signals generated by molecular clustering can influence cell spreading and motility via familiar transduction pathways. Although it is not yet possible to reconstruct with confidence the entire sequence of events between initial glycoprotein clustering and motility, there is a lot of information which points to the identities of the molecular ingredients. I shall focus the discussion on the thin peripheral lamellar extensions produced by cell types ranging from amoebae to vertebrate nerve growth cones, and discuss the experimental evidence relating to their cytoskeletal architecture and dynamics. Finally I shall try to construct models of motility consistent with the experimental data, and suggest how lamellar motility may be modulated by signals generated by clustered adhesion molecules.
Gingell
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Department of Anatomy and Developmental Biology, University College London, UK.
D000818:Animals; D002448:Cell Adhesion / Q000502:physiology; D002450:Cell Communication / Q000502:physiology*; D002465:Cell Movement / Q000502:physiology*; D005109:Extracellular Matrix / Q000502:physiology*; D006023:Glycoproteins / Q000502:physiology; D006801:Humans; D008954:Models, Biological; D015398:Signal Transduction / Q000502:physiology
D006023:Glycoproteins