Intercellular communication and the control of growth: XI. Alteration of junctional permeability by the src gene in a revertant cell with normal cytoskeleton.
To learn whether the reduction of cell-to-cell communication in transformation is a possible primary effect of pp60src phosphorylation or secondary to a cytoskeletal alteration, we examined the junctional permeability in transformed cells with normal cytoskeleton. The permeability to fluorescent-labelled mono- and diglutamate was compared in clones of Faras' vole cells--clones transformed by Rous sarcoma virus and reverted from that transformation. One revertant clone (partial revertant), had the high level of pp60src kinase activity and tumorigenicity of the fully transformed parent clone, but had lost the cytoskeletal alterations of that clone. Another revertant clone (full revertant) had lost the tumorigenicity and most of the pp60src kinase activity, in addition (J.F. Nawrocki et al., 1984, Mol. Cell Biol. 4:212). The junctional permeability of the partial revertant with normal cytoskeleton was similar to that of the fully transformed parent clone with abnormal cytoskeleton. The permeabilities of both were lower than those of the full revertant and the normal uninfected cell, demonstrating that the junctional change by the src gene is independent of the cytoskeletal one.
D000818:Animals; D003411:Arvicolinae; D001358:Avian Sarcoma Viruses; D002450:Cell Communication; D002455:Cell Division; D002472:Cell Transformation, Viral; D002478:Cells, Cultured; D003599:Cytoskeleton / Q000648:ultrastructure*; D007365:Intercellular Junctions / Q000502:physiology*; D015688:Oncogene Protein pp60(v-src); D009857:Oncogenes; D014764:Viral Proteins / Q000502:physiology
D014764:Viral Proteins; D015688:Oncogene Protein pp60(v-src)