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Significance Dual leucine-zipper kinase (DLK) is essential for responses to nerve injury and subsequent neural regeneration by controlling transfer of signals from damaged distal axons to neuronal cell bodies. However, DLK is predicted to be freely diffusible, raising the question of how it conveys long-distance, directional signals. Here we report that direct modification of DLK with the lipid palmitate, a process called palmitoylation, is critical for retrograde injury signaling. At the molecular level, palmitoylation targets DLK to retrograde trafficking vesicles, assembles DLK-dependent signaling complexes, and is also essential for DLK kinase activity. This “multifunctional” palmitoylation explains how DLK mediates injury responses and may be a previously unappreciated mechanism that ensures the specificity of enzymatic signaling in diverse cell types.

Palmitoylation controls DLK localization, interactions and activity to ensure effective axonal injury signaling