Biology subjects

royet, j.

Publications and source records attributed to royet, j..

2 recordsLinked to original sources

bioRxiv2025

Uracil-Driven ROS signals activate larval TrpA1-B neurons to prime the Drosophila adult gustatory response to bacterial signal

Animals perceive their environment through their sensory systems why rely on neuronal circuits and proteins, but can be modulated by internal physiological conditions or exogenous factors. We have shown that the presence of certain pathogenic bacteria in the larval gut can alter the specificity of bacterial peptidoglycan recognition in the adults that emerge from these larvae. However, the nature of the bacterial signal and the host cells and molecules involved in receiving and transducing this signal remained unknown. We identify here uracil as the bacterial metabolite responsible for this priming and demonstrate that the effect is mediated by Duox-dependent production of reactive oxygen species in the larval gut. We show that specific expression of TrpA1 isoforms in a Gr66a-expressing neuron of the larval terminal organ is required for the adult response. Together, these findings reveal uracil as the bacterial cue and the Duox/ROS and TrpA1/Gr66a modules as key mediators linking larval gut microbial signals and host integration to subsequent sensory system modulation in the adult. HighlightsO_LIBacterial uracil primes larvae to drive adult aversion to peptidoglycan C_LIO_LIDuox-dependent ROS in larval enterocytes are required for sensory priming C_LIO_LITrpA1 B/C/E isoforms in a larval Gr66a+ neuron mediate priming C_LIO_LIUracil induces Duox/ROS signals enabling inter-larval activation of TrpA1-B+ neurons C_LI

neuroscience↗

bioRxiv2021

Microbiota-dependent inflammation promotes metabolic disorder via NF-kB-mediated inhibition of SREBP in Drosophila adipocytes

Bacteria that colonize eukaryotic gut have profound influences on the physiology of their host. In Drosophila, many of these effects are mediated by the adipocytes that combine immune and metabolic functions. We show here that gut colonization by specific bacteria species stimulate lipogenesis in surrounding enterocytes but also in remote fat body cells and ovaries. This bacteria-dependent lipid production is mediated by SREBP and requires a functional insulin signaling. However, it is antagonized by microbiota-born peptidoglycan which by activating NF-{kappa}B signaling, cell-autonomously represses SREPP activation in adipocytes but not in enterocytes. We finally show that by reducing microbiota-derived PGN, the gut-produced PGRP-LB amidase balances host immune and metabolic responses of the fat body to gut-associated bacteria. In the absence of such modulation, uncontrolled immune pathway activation prevents lipid production by the fat body resulting in infection-dependent host death. BulletsO_LIGut microbiota activates lipogenesis locally in enterocytes and remotely in adipocytes C_LIO_LIBacteria-dependent activation of SREBP in adipocytes is mediated by insulin signaling C_LIO_LIActivation of lipid synthesis by microbiota is antagonized by NF-{kappa}B signaling triggered by gut-born peptidoglycan C_LIO_LIBy reducing peptidoglycan circulating levels, PGRP-LB maintains a balance between immune and metabolic response to microbiota C_LI

physiology↗