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• W2596859113 abstract "Patricia F. Mane% and Robert C. Walsh, Jr. Department of Biochemistry University of North Carolina Chapel Hill, North Carolina 27514 Summary Dihydrocytochalasin B (HXB) disrupts the actin structure of Swiss/ST3 mouse fibroblasts and in- hibits the ability of serum growth factors to stimu- late DNA synthesis in quiescent cultures. Low doses of HB by epidermal growth factor and insulin; or by epidermal growth factor, fibroblast growth factor and insulin. HB Friedkin et al., 1979; McClain and Edelman, 1980). The suggestion that microfilaments might also be involved in mediating growth control signals is based partly on electron microscopic evidence that a significant fraction of the cell’s microfilaments are organized in dense meshworks that lie directly under the plasma membrane (Wolosewick and Porter, 1976), where they could presumably interact with membrane receptors for growth factors and with nearby microtubules. Additional support for the in- volvement of actin-containing elements in growth con- trol derives from numerous studies of cells trans- formed by tumor viruses, most of which have shown that a disruption of actin microfilament bundles is expressed coordinately with the loss of serum- and anchorage-dependent growth (reviewed by Maness, 1981). Direct evidence for a part played by microfila- ments in the transmission of growth signals has been lacking, however, because unlike colchicine and col- cemid, which specifically inhibit microtubule polym- erization, drugs capable of specifically disrupting actin structures have not been available until recently. Dihydrocytochalasin B (HB MacLean-Fletcher and Pollard, 1980). In vivo, cytochalasin B and H&B produce pronounced effects on cell shape and inhibit cellular motile proc- esses, including cytokinesis. Cytochalasin B is less specific than H&B because it also acts as a potent inhibitor of hexose transport, apparently by binding to a component of the hexose transporter (Salter and Weber, 1979). H&B does not interfere with glucose uptake at comparable concentrations (1-l 0 PM) (At- las and Lin, 1978). We took advantage of the selective effect of H&B on actin-related processes to examine the role of the actin cytoskeleton in cell growth control. We used H&B to test the hypothesis that an intact actin cytoskeleton is required for initiation of DNA synthesis, using nonconfluent Swiss/3T3 mouse fi- broblasts stimulated to proliferate from quiescence by the addition of serum or purified serum growth factors. Under these conditions it was essential to use an actin-specific reagent that did not affect glucose transport, since glucose has been shown to control directly the proliferation nonconfluent 3T3 cells stimulated from a state of quiescence (Holley and Kiernan, 1974). Under other culture conditions, how- ever, the rate of glucose uptake may not affect prolif- eration (Naiditch and Cunningham, 1977). We found that H&B at low concentrations (2-10 x 10e7 M) blocks initiation of DNA synthesis in 3T3 cells. At concentrations that block initiation, H&B causes major changes in cellular actin structure and cell shape but does not interfere with glucose or thymidine transport. Cells transformed by SV40 or Moloney murine sarcoma virus were unresponsive to growth inhibition by H&B. The results suggest that a functional actin cytoskeleton is required to transmit growth factor signals for cell cycle initiation in normal cells, but in transformed cells, in which the serum growth factor requirement is reduced, the actin-de- pendent step is obviated." @default.
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• W2596859113 date "1982-01-01" @default.
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• W2596859113 title "and Inhibits Initiation of DNA Synthesis in 3T3 Cells" @default.
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