Cytochalasin B induces polarisation of plasma membrane components and actin in transformed cells

Kg, Sundqvist; Otteskog, Per

doi:10.1038/274915a0

Cited by 18 publications

(7 citation statements)

References 17 publications

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“…It is not at all clear at the molecular level how CB treatment can cause the striking glycoprotein relocalization observed in L-929 and other cell types (27,28). Relocalization is unlikely to be caused by a direct interaction of CB with cell surface glycoproteins.…”

Section: Discussionmentioning

confidence: 92%

“…The CBinduced redistribution of/32-microglobulin is reversible and it is inhibited by colchicine. CB is found to promote a similar relocalization of H-2 antigens in transformed 3T3 cells (28), /32-microglobulin in HeLa cells, and measles virus hemaglutinin in persistently infected Lu 106 cells (27).…”

mentioning

confidence: 89%

“…Colchicine does not affect the cytoplasmic contraction or bleb formation promoted by the cytochalasins, but it blocks aggregation of blebs into clusters (17, 27). All morphologic effects of the cytochalasins are reversible when the drug is withdrawn from the cell growth medium (22,26).Sundquist and his colleagues (27,28) have demonstrated that CB-induced changes in cell surface morphology are accompanied by an equally dramatic relocalization of certain cell surface proteins. The case of surface ~2-microglobulin in Lu 106 (transformed human lung) cells is illustrative.…”

mentioning

confidence: 99%

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Site-specific maturation of enveloped viruses in L cells treated with cytochalasin B.

Brown¹,

Salomonsky²

1985

The Journal of Cell Biology

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Treatment of infected L cells with 10 micrograms/ml cytochalasin B (CB) was found to promote a rapid relocalization of viral glycoproteins on the cell surface. Whereas the vesicular stomatitis virus G protein and the influenza virus hemagglutinin were uniformly distributed on the surface of untreated cells, in CB-treated cells, they were strikingly concentrated at cell extremities in the regions of clustered blebs. Glycoprotein concentration at cell extremities was accompanied by preferential maturation of virus particles from the same sites; both vesicular stomatitis and influenza viruses budded predominantly from the vicinity of clustered blebs. This effect of CB was completely reversible. Removal of CB from the cell growth medium resulted in a return of viral glycoproteins to the uniform distribution characteristic of untreated cells and to uniform virus budding. The results of this study are interpreted in terms of a model that suggests that preferential budding of viruses from the regions of bleb clusters is due to the concentration of viral glycoproteins at these sites.

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Section: Discussionmentioning

confidence: 92%

mentioning

confidence: 89%

mentioning

confidence: 99%

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Site-specific maturation of enveloped viruses in L cells treated with cytochalasin B.

Brown¹,

Salomonsky²

1985

The Journal of Cell Biology

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“…This may be explained by the well known property of this dnlg to disrupt microfilaments and to produce extensions (3, t7). Finally the eytoptasma retracts (9,26,30). It is remarkable that cells infected with strains of HSV wodueing celt rounding retain the ability to respond to Cytochal~sine ]3 by forming protuberances.…”

Section: Discussionmentioning

confidence: 95%

Microtubules and microfilaments in HSV-infected rabbit-kidney cells

Heeg

Haase

Brauer

et al. 1981

Archives of Virology

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In rabbit kidney cells infected with strains of Herpes simplex virus producing either cell-rounding or polycaryocytosis. Vinblastine induced paracrystals. This could be shown by phase-contrast- and electron-microscopy. Infections were done under one-step-growth conditions or at low MOI. 90 per cent noninfected cells contained stress fibers as detected by Servablue R250-staining. Shortly after recruitment into polycaryocytes, stress fibres of normal length appearing in criss-cross arrangement can be seen in the periphery of these cells. Later they polymerize to very long fibers and finally they are partially destroyed. The time of destruction depends on the MOI employed. By using Actinomycin D and/or Cycloheximide as blocking agents, it could be shown that polymerization of microfilaments correlates in time with giant cell formation. In view of the fact that the virus synthesis is accompanied in parallel by a special rearrangement of microfilaments as well as polycaryocytosis, both these processes have to be considered as caused by early (and late ?) protein-synthesis (beta-/gamma-proteins) but not as induced by "very-early" proteins (alpha-proteins).

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“…On the other hand, there was no difference observed in the isoactin forms seen in homogenates from each cell type. Thus, by these criteria, the results suggest that the observed differences in capping properties among the cells were not due to qualitative variation among the actin forms; rather the capping response in the alveolar macrophage may depend upon a unique topographical relationship of microfilaments to the membrane (4) which may be amenable to perturbation by altering the metabolism of the phagocytic cells as has been seen in virally infected or transformed cells (12,13). The biological basis of capping in cells of various types is not known, but differences in this parameter such as those shown here may ultimately be related to cell differentiation and metabolism.…”

mentioning

confidence: 89%

Metabolic and Structural Requirements for Concanavalin A Capping in Phagocytic Cells

Williams

Lessard

Boxer

et al. 1979

Experimental Biology and Medicine

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Cytochalasin B induces polarisation of plasma membrane components and actin in transformed cells

Cited by 18 publications

References 17 publications

Site-specific maturation of enveloped viruses in L cells treated with cytochalasin B.

Site-specific maturation of enveloped viruses in L cells treated with cytochalasin B.

Microtubules and microfilaments in HSV-infected rabbit-kidney cells

Metabolic and Structural Requirements for Concanavalin A Capping in Phagocytic Cells

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