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J Biol Chem, Vol. 273, Issue 43, 27816-27823, October 23, 1998

Regulation of Apoptosis by alpha -Subunits of G12 and G13 Proteins via Apoptosis Signal-regulating Kinase-1

Yuliya V. BerestetskayaDagger , Michel P. Faure§, Hidenori Ichijo, and Tatyana A. Voyno-YasenetskayaDagger

From the Dagger  Department of Pharmacology, University of Illinois, Chicago, Illinois 60612, § Sugen, Inc., Redwood City, California 94063, and the  Department of Oral Pathology, Cancer Institute, Tokyo 113, Japan

Many growth factors and G protein-coupled receptors activate mitogen-activated protein (MAP) kinase pathways. The MAP kinase pathways are involved in the regulation of the ubiquitous process of apoptosis or programmed cell death. Two related MAP kinase kinase kinases, apoptosis-signal regulating kinase 1 (ASK1) and MAP kinase kinase kinase 1 (MEKK1), stimulate c-Jun kinase (JNK) activity and induce apoptosis. Transient transfection of dominant negative and constitutively active components of the JNK pathway in COS-7 cells showed that two G protein subunits, Galpha 12 and Galpha 13, stimulated the JNK pathway in a ASK1- and MEKK1-dependent manner. Moreover, the mutationally activated Galpha 12 and Galpha 13 stimulated the kinase activity of ASK1. Both Galpha 12 and Galpha 13 employ small GTPases, Cdc42 and Rac1, to transduce signal to MEKK1 and, subsequently, to JNK. However, activation of JNK by Cdc42 and Rac1 did not require ASK1. Additionally, ASK1 and MEKK1 are involved in the apoptosis induced by Galpha 12 and Galpha 13. We conclude that Galpha 12 and Galpha 13 can induce apoptosis using two separate MAP kinase pathways; one is initiated by ASK1, and the other is initiated by MEKK1. Furthermore, Bcl-2 can block apoptosis induced by Galpha 12 and Galpha 13. This death-sparing function was associated with increased Bcl-2 phosphorylation, suggesting that phosphorylation of Bcl-2 may be a critical mechanism protecting cells from Galpha 12- and Galpha 13-induced apoptosis.

Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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