Requirement of JNK for Stress- Induced Activation of the Cytochrome c-Mediated Death Pathway

TLDR

JNK is activated by ultraviolet radiation, but its role in UV‑induced cell death had not been clarified. Loss of JNK protects primary murine embryonic fibroblasts from UV‑induced apoptosis by blocking mitochondrial cytochrome c release, demonstrating that JNK is essential for UV‑triggered mitochondrial death signaling.

Abstract

The c-Jun NH 2 -terminal kinase (JNK) is activated when cells are exposed to ultraviolet (UV) radiation. However, the functional consequence of JNK activation in UV-irradiated cells has not been established. It is shown here that JNK is required for UV-induced apoptosis in primary murine embryonic fibroblasts. Fibroblasts with simultaneous targeted disruptions of all the functional Jnk genes were protected against UV-stimulated apoptosis. The absence of JNK caused a defect in the mitochondrial death signaling pathway, including the failure to release cytochrome c. These data indicate that mitochondria are influenced by proapoptotic signal transduction through the JNK pathway.