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Abstract
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.
We thank S. Korsmeyer for providing Bid−/− fibroblasts; N. Ahn for providing the activated MEK1 expression vector; T. Barrett, S. Stone, and S. A. Quail for technical assistance; and K. Gemme for administrative assistance.
This study was supported in part by grant CA65861 from the National Cancer Institute. R.A.F. and R.J.D. are investigators of the Howard Hughes Medical Institute.