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 an...

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Bibliographic Details
Published in:Current biology 1998-08, Vol.8 (17), p.967,S1-970,S1
Main Authors: Eby, Jennifer J., Holly, Stephen P., van Drogen, Frank, Grishin, Anatoly V., Peter, Matthias, Drubin, David G., Blumer, Kendall J.
Format: Article
Language:English
Subjects:
Actins - metabolism
Calcium-Calmodulin-Dependent Protein Kinases - physiology
cdc42 GTP-Binding Protein, Saccharomyces cerevisiae
Cell Cycle Proteins - genetics
Cell Cycle Proteins - physiology
Cell Polarity
Cytoskeleton - enzymology
Cytoskeleton - metabolism
GTP-Binding Proteins - genetics
GTP-Binding Proteins - physiology
Intracellular Signaling Peptides and Proteins
MAP Kinase Kinase Kinases
Mutation
Protein-Serine-Threonine Kinases - genetics
Protein-Serine-Threonine Kinases - physiology
Recombinant Proteins
Saccharomyces cerevisiae
Saccharomyces cerevisiae - cytology
Saccharomyces cerevisiae - enzymology
Saccharomyces cerevisiae - genetics
Saccharomyces cerevisiae Proteins
Signal Transduction
Temperature
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Summary: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.
ISSN:0960-9822
1879-0445
DOI:10.1016/S0960-9822(98)00398-4