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PMID: 8898204 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Rac and Cdc42 induce actin polymerization and G1 cell cycle progression independently of p65PAK and the JNK/SAPK MAP kinase cascade.

Cell ·Vol. 87 ·No. 3 ·1996-11-01 ·Pages 519-29

Lamarche N, Tapon N, Stowers L, Burbelo PD, Aspenström P, Bridges T, Chant J, Hall A

Abstract

Rac and Cdc42 regulate a variety of responses in mammalian cells including formation of lamellipodia and filopodia, activation of the JNK MAP kinase cascade, and induction of G1 cell cycle progression. Rac is also one of the downstream targets required for Ras-induced malignant transformation. Rac and Cdc42 containing a Y40C effector site substitution no longer intact with the Ser/Thr kinase p65PAK and are unable to activate the JNK MAP kinase pathway. However, they still induce cytoskeletal changes and G1 cell cycle progression. Rac containing an F37A effector site substitution, on the other hand, no longer interacts with the Ser/Thr kinase p160ROCK and is unable to induce lamellipodia or G1 progression. We conclude that Rac and Cdc42 control MAP kinase pathways and actin cytoskeleton organization independently through distinct downstream targets.

MeSH Terms

3T3 Cells Actins/metabolism Animals COS Cells Calcium-Calmodulin-Dependent Protein Kinases/physiology Cell Cycle Proteins/physiology Cytoskeleton/metabolism,ultrastructure DNA Replication Enzyme Activation G1 Phase/physiology GTP Phosphohydrolases/metabolism GTP-Binding Proteins/physiology GTPase-Activating Proteins Integrins/metabolism JNK Mitogen-Activated Protein Kinases MAP Kinase Kinase 4 Mice Mitogen-Activated Protein Kinase Kinases Mutagenesis, Site-Directed Phosphorylation Polymers Protein Kinases/physiology Protein Processing, Post-Translational Protein Serine-Threonine Kinases/physiology Proteins/genetics,physiology Pseudopodia/ultrastructure Recombinant Fusion Proteins/metabolism Signal Transduction/physiology Transfection cdc42 GTP-Binding Protein p21-Activated Kinases ras GTPase-Activating Proteins

Chemicals

Actins Cell Cycle Proteins GTPase-Activating Proteins Integrins Polymers Proteins Recombinant Fusion Proteins ras GTPase-Activating Proteins Protein Kinases Protein Serine-Threonine Kinases p21-Activated Kinases Calcium-Calmodulin-Dependent Protein Kinases JNK Mitogen-Activated Protein Kinases MAP Kinase Kinase 4 Map2k4 protein, mouse Mitogen-Activated Protein Kinase Kinases GTP Phosphohydrolases GTP-Binding Proteins cdc42 GTP-Binding Protein

Authors & Affiliations

8 authors, click to expand affiliations / ORCID

Lamarche N

Department of Biochemistry, University College London, United Kingdom.

Tapon N

Stowers L

Burbelo P D

Aspenström P

Bridges T

Chant J

Hall A

Article Info

Journal

Cell

Abbr.

Cell

ISSN

0092-8674

DOI

10.1016/s0092-8674(00)81371-9

Published

1996-11-01

Pages

519-29

Language

English

Region

United States

NLM ID

0413066

Subset

Grants

Wellcome Trust · United Kingdom

External Links

PubMed source DOI: 10.1016/s0092-8674(00)81371-9 View journal details

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Rac and Cdc42 induce actin polymerization and G1 cell cycle progression independently of p65PAK and the JNK/SAPK MAP kinase cascade.

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