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

ABSTRACT: Summary 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 Drosophila. Using a genetic tissue repair system in Drosophila 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 TkR86C 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 TkR86C hampered injury-dependent changes in the expression of vermillion 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. Graphical abstract Highlights • Neuronal TkR86C is remotely required for Drosophila wing disc repair• TkR86C-RNAi in neuron remotely impairs injury-induced Kyn metabolic changes• KynA treatment recovers the wing phenotype induced by neuronal knockdown of TkR86C Cellular neuroscience; Molecular physiology

SUBMITTER: Kashio S

PROVIDER: S-EPMC10457576 | biostudies-literature | 2023 Aug

REPOSITORIES: biostudies-literature

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