The detection of bacteria by Drosophila immune cells activates the NF-κB signaling pathway and triggers the production of antibacterial molecules. The sustained activation of this molecular cascade is harmful to the host and hence regulated at several levels by antagonist proteins. In an article published in PLoS Genetics, Julien Royet’s team shows that the inactivation of one of these repressors (PGRP-LF) causes, as expected, the constitutive production of antimicrobial molecules by the host. The results show that, more surprisingly, this activation is also taking place under axenic conditions that is to say in the complete absence of immune stimuli. Moreover, flies mutant for this repressor exhibit important developmental defects when raised in axenic conditions. Genetic evidence demonstrates that uncontrolled activation of the NF-κB pathway in PGRP-LF mutants prevents apoptosis-dependent developmental processes from proceeding normally. This work that suggests the existence of endogenous ligands for the NF-κB pathway underlines the close links between immune response and development in this model insect.
Inhibition of a NF-κB/Diap1 Pathway by PGRP-LF Is Required for Proper Apoptosis during Drosophila Development
Raphael Tavignot, Delphine Chaduli, Fatoumata Djitte, Bernard Charroux, Julien Royet
PLoS Genet. 2017 Jan 13;13(1):e1006569.
Bernard Charroux (Bernard.firstname.lastname@example.org)
Julien Royet (Julien.email@example.com)