Active JNK (green) rides with dynein (red) back to the cell body.
JNK and syd were found in murine axons on vesicles that were traveling both out to axon tips (on kinesin motors) and back to the cell body (on dynein). Injuries activated JNK out in axons and enhanced its interaction with the dynein-associated complex dynactin. Axonal injuries are thus expected to bring active JNK to the cell body, where it can turn on c-Jun to start the repair process.
Other molecules in complex with JNK may keep the kinase in its activated form for the long trip, either by protecting JNK's initial phosphorylation or by repeatedly phosphorylating it. As yet, though, it is unclear what other proteins reside in the vesicles. JNK and syd may be simply hitchhiking on vesicles that are transporting synaptic proteins. Alternatively, the vesicles may be dedicated damage repair packages. A cell culture model will be most helpful for the biochemistry that needs to be done next.
Neurons may be an extreme version of a problem that also exists in smaller cells. Although microtubules are not absolutely required for injury responses in epithelial cells, a motor-based transport mechanism may be used normally to improve repair efficiency.