Negative regulator of epidermal barrier repair and innate immune responses to wounding (PubMed:19164535, PubMed:27661253). The role in epidermal tissue integrity and wound healing is established through the inhibition of epidermal microtubule stability, possibly via the negative regulation of the microtubule minus-end binding protein ptrn-1 (PubMed:27661253). In epidermis, prevents expression of specific unc-44 isoforms probably by promoting nuclear localization of pinn-1, which in turn may affect sydn-1-ssup-72-mediated regulation of alternative polyadenylation of unc-44 mRNA (PubMed:28087624). Appears to act downstream of or in parallel to muscarinic signaling in the regulation of autophagy (PubMed:17785524). ATP + L-seryl-[protein] = ADP + H(+) + O-phospho-L-seryl-[protein] ATP + L-threonyl-[protein] = ADP + H(+) + O-phospho-L-threonyl-[protein] Interacts with ptrn-1. Exhibits movement along microtubules. Expressed in epidermis, muscles and neurons. Present from late embryogenesis onwards. Beginning in the L3 stage, animals display striking and progressive defects in morphology of the epidermis and cuticle in several body regions, particularly in the nose, tail, vulva, and the dorsal midline in the region of the posterior pharyngeal bulb (PubMed:19164535, PubMed:27661253). The cuticle in these regions becomes up to 5-10 times thicker than the wild-type, at the expense of underlying epidermis (PubMed:19164535, PubMed:27661253). Up-regulates innate immune responses to damage (PubMed:19164535). Decreases starvation-induced autophagy (PubMed:17785524). Disorganization and hyper-stabilization of epidermal microtubules and reduced microtubule growth rates (PubMed:27661253). Treatment with a microtubule stabilizing drug, paclitaxel, results in enhanced epidermal morphology defects (PubMed:27661253). In a ptrn-1 mutant background, suppression of the epidermal morphology defects (PubMed:27661253). Belongs to the protein kinase superfamily. CAMK Ser/Thr protein kinase family. DAP kinase subfamily.