Article: article from journal or magazin.
Actin cytoskeleton organization regulated by the PAK family of protein kinases.
Cdc42, Rac1 and other Rho-type GTPases regulate gene expression, cell proliferation and cytoskeletal architecture [1,2]. A challenge is to identify the effectors of Cdc42 and Rac1 that mediate these biological responses. Protein kinases of the p21-activated kinase (PAK) family bind activated Rac1 and Cdc42, and switch on mitogen-activated protein (MAP) kinase pathways; however, their roles in regulating actin cytoskeleton organization have not been clearly established [3-5]. Here, we show that mutants of the budding yeast Saccharomyces cerevisiae lacking the PAK homologs Ste20 and Cla4 exhibit actin cytoskeletal defects, in vivo and in vitro, that resemble those of cdc42-1 mutants. Moreover, STE20 overexpression suppresses cdc42-1 growth defects and cytoskeletal defects in vivo, and Ste20 kinase corrects the actin-assembly defects of permeabilized cdc42-1 cells in vitro. Thus, PAKs are effectors of Cdc42 in pathways that regulate the organization of the cortical actin cytoskeleton.
Actins/metabolism, Calcium-Calmodulin-Dependent Protein Kinases/physiology, Cell Cycle Proteins/genetics, Cell Cycle Proteins/physiology, Cell Polarity, Cytoskeleton/enzymology, Cytoskeleton/metabolism, GTP-Binding Proteins/genetics, GTP-Binding Proteins/physiology, Mutation, Protein-Serine-Threonine Kinases/genetics, Protein-Serine-Threonine Kinases/physiology, Recombinant Proteins, Saccharomyces cerevisiae/cytology, Saccharomyces cerevisiae/enzymology, Saccharomyces cerevisiae Proteins, Signal Transduction, Temperature, cdc42 GTP-Binding Protein, Saccharomyces cerevisiae
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