Sean R Cuddy, Austin R Schinlever ... Anna R Cliffe
Herpes simplex virus reactivates from a latent infection when neurons become hyperexcitable in response to an inflammatory cytokine known to be released during fever and stress.
Alexandra B Byrne, Rebecca D McWhirter ... Marc Hammarlund
In C. elegans and mouse neurons, the balance between poly(ADP-ribose) glycohydrolases and poly(ADP-ribose) polymerases regulates axon regeneration downstream of DLK-1/MAPKKK signaling.
Genetic, developmental and pharmacological analysis in Caenorhabditis elegans demonstrate that ATAT-2 tubulin acetyltransferase activity regulates synapse maintenance by acting within the RPM-1 signaling network, but independent of the DLK-1 MAP3K.
Axonal damage sensing kinase DLK is a direct target and mediator of the cAMP effector kinase PKA in a unified mechanism for stimulating axonal regeneration.
Synaptic defects previously attributed to loss of kinesin function are found to be mediated by the Wnd/DLK axonal injury signaling pathway, which restrains the total levels of presynaptic proteins in response to their accumulation.