Involvement of neuronal tachykinin-like receptor at 86C in disc repair via regulation of kynurenine metabolism.

Neurons contribute to the regeneration of projected tissues; however, it remains unclear whether they are involved in the non-innervated tissue regeneration. Herein, we showed that a neuronal tachykinin-like receptor at 86C (TkR86C) is required for the repair of non-innervated wing discs in . Using a genetic tissue repair system in larvae, we performed genetic screening for G protein-coupled receptors to search for signal mediatory systems for remote tissue repair. An evolutionarily conserved neuroinflammatory receptor, TkR86C, was identified as the candidate receptor. Neuron-specific knockdown of impaired disc repair without affecting normal development. We investigated the humoral metabolites of the kynurenine (Kyn) pathway regulated in the fat body because of their role as tissue repair-mediating factors. Neuronal knockdown of hampered injury-dependent changes in the expression of in the fat body and humoral Kyn metabolites. Our data indicate the involvement of TkR86C neurons upstream of Kyn metabolism in non-autonomous tissue regeneration.