The problem was that other cells possess the closely related genes, Jnk1 and Jnk2, and knocking out only one produces no detectable effect. On the other hand, knocking out both genes causes death very early during embryogenesis. In a five-year effort, the scientists solved the problem by learning to isolate and culture mouse embryonic fibroblast cells that lacked both genes. What's more, we were also able to take this finding a step further and establish how Jnk fits into the apoptosis pathway discovered by Xiaodong Wang. Wang, an HHMI investigator at the University of Texas Southwestern Medical Center at Dallas, discovered that the release of an energy-carrying molecule called cytochrome c from the cells' mitochondria is the key molecular event that triggers cell death.
Mitochondria are the energy-producing powerhouses of the cell.
Biochemical studies by Davis and his colleagues revealed that JNK-deficient cells exposed to UV light failed to release cytochrome c from their mitochondria. It's important because JNK's role in apoptosis was controversial. This finding serves to fit JNK into an existing and established apoptosis mechanism. The researchers are also exploring the differences between the enzymes produced by Jnk1 and Jnk2, both of which seem to play roles in cell proliferation in addition to apoptosis. The two genes are expressed throughout the body, and in most situations they seem to have a very similar function.