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The small GTP-binding protein rac regulates growth factor-induced membrane ruffling.

Abstract

The function of rac, a ras-related GTP-binding protein, was investigated in fibroblasts by microinjection. In confluent serum-starved Swiss 3T3 cells, rac1 rapidly stimulated actin filament accumulation at the plasma membrane, forming membrane ruffles. Several growth factors and activated H-ras also induced membrane ruffling, and this response was prevented by a dominant inhibitory mutant rac protein, N17rac1. This suggests that endogenous rac proteins are required for growth factor-induced membrane ruffling. In addition to membrane ruffling, a later response to both rac1 microinjection and some growth factors was the formation of actin stress fibers, a process requiring endogenous rho proteins. Using N17rac1 we have shown that these growth factors act through rac to stimulate this rho-dependent response. We propose that rac and rho are essential components of signal transduction pathways linking growth factors to the organization of polymerized actin.

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  • Publisher Full Text
  • Authors+Show Affiliations

    ,

    Institute for Cancer Research, Chester Beatty Laboratories, London, England.

    , , ,

    Source

    Cell 70:3 1992 Aug 7 pg 401-10

    MeSH

    3T3 Cells
    Actins
    Animals
    Cell Adhesion
    Cell Membrane
    Culture Media, Serum-Free
    Cytoskeleton
    Fluorescent Antibody Technique
    GTP-Binding Proteins
    Growth Substances
    Guanosine Diphosphate
    Guanosine Triphosphate
    Mice
    Oncogene Protein p21(ras)
    Pinocytosis
    Substrate Specificity
    rac GTP-Binding Proteins

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    1643658

    Citation

    TY - JOUR T1 - The small GTP-binding protein rac regulates growth factor-induced membrane ruffling. AU - Ridley,A J, AU - Paterson,H F, AU - Johnston,C L, AU - Diekmann,D, AU - Hall,A, PY - 1992/8/7/pubmed PY - 1992/8/7/medline PY - 1992/8/7/entrez SP - 401 EP - 10 JF - Cell JO - Cell VL - 70 IS - 3 N2 - The function of rac, a ras-related GTP-binding protein, was investigated in fibroblasts by microinjection. In confluent serum-starved Swiss 3T3 cells, rac1 rapidly stimulated actin filament accumulation at the plasma membrane, forming membrane ruffles. Several growth factors and activated H-ras also induced membrane ruffling, and this response was prevented by a dominant inhibitory mutant rac protein, N17rac1. This suggests that endogenous rac proteins are required for growth factor-induced membrane ruffling. In addition to membrane ruffling, a later response to both rac1 microinjection and some growth factors was the formation of actin stress fibers, a process requiring endogenous rho proteins. Using N17rac1 we have shown that these growth factors act through rac to stimulate this rho-dependent response. We propose that rac and rho are essential components of signal transduction pathways linking growth factors to the organization of polymerized actin. SN - 0092-8674 UR - https://www.unboundmedicine.com/medline/citation/1643658/The_small_GTP_binding_protein_rac_regulates_growth_factor_induced_membrane_ruffling_ L2 - http://linkinghub.elsevier.com/retrieve/pii/0092-8674(92)90164-8 ER -