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Molecular and Cellular Biology, July 2002, p. 4929-4942, Vol. 22, No. 13
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.13.4929-4942.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

The Bax Subfamily of Bcl2-Related Proteins Is Essential for Apoptotic Signal Transduction by c-Jun NH2-Terminal Kinase

Kui Lei,1 Anjaruwee Nimnual,2 Wei-Xing Zong,3 Norman J. Kennedy,1 Richard A. Flavell,4 Craig B. Thompson,3 Dafna Bar-Sagi,2 and Roger J. Davis1*

Howard Hughes Medical Institute and Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605,1 Department of Molecular Genetics and Microbiology, State University of New York at Stony Brook, Stony Brook, New York 11794,2 Abramson Family Cancer Research Institute, Department of Cancer Biology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104,3 Howard Hughes Medical Institute and Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 065204

Received 6 December 2001/ Returned for modification 30 January 2002/ Accepted 7 April 2002

Targeted gene disruption studies have established that the c-Jun NH2-terminal kinase (JNK) signaling pathway is required for stress-induced release of mitochondrial cytochrome c and apoptosis. Here we demonstrate that activated JNK is sufficient to induce rapid cytochrome c release and apoptosis. However, activated JNK fails to cause death in cells deficient of members of the Bax subfamily of proapoptotic Bcl2-related proteins. Furthermore, exposure to stress fails to activate Bax, cause cytochrome c release, and induce death in JNK-deficient cells. These data demonstrate that proapoptotic members of the Bax protein subfamily are essential for JNK-dependent apoptosis.

* Corresponding author. Mailing address: Howard Hughes Medical Institute, Program in Molecular Medicine, University of Massachusetts Medical School, 373 Plantation St., Worcester, MA 01605. Phone: (508) 856-6054. Fax: (508) 856-3210. E-mail: Roger.Davis{at}Umassmed.Edu.

Molecular and Cellular Biology, July 2002, p. 4929-4942, Vol. 22, No. 13
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.13.4929-4942.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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