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

Soshiro Kashio; Shu Masuda; Masayuki Miura

doi:10.1016/j.isci.2023.107553

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

iScience. 2023 Aug 7;26(9):107553. doi: 10.1016/j.isci.2023.107553. eCollection 2023 Sep 15.

Authors

Soshiro Kashio¹, Shu Masuda¹, Masayuki Miura¹

Affiliation

¹ Department of Genetics, Graduate School of Pharmaceutical Sciences, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.

Abstract

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.

Keywords: Cellular neuroscience; Molecular physiology.