(A) Schematic representation of the Drosophila IMD pathway. Peptidoglycan (PGN) released by bacteria is recognized at the cell membrane by PGRP-LC or inside the cell by PGRP-LE. This PGRP/PGN interaction triggers via IMD, FADD, DREDD, nuclear translocation of Relish. Extracellular PGRP with amidase activity, such as PGRP-LBPC, dampens this signaling by degrading PGN. (B) Septic injury impairs egg-laying capacity in wild-type females. Pictures of fly tubes seen from the top. The blue dye is used to facilitate quantification of the eggs that appear as white dots. (C) Septic injury transiently impairs egg-laying capacity in wild type and in PGRP-LB mutant females. The egg-laying ratio for a time window (6 hr or 24 hr) corresponds to the number of eggs laid by a female after infection over the number of eggs laid by control female of the same genotype. (D and E) Injection of highly purified PGN in wt (D, E) and PGRP-LB mutants (E) is sufficient to reduce egg laying. (F) Mutation in Relish or in Dredd is preventing egg laying decrease post-infection. (G) Epistatic analyses showing that mutations in PGRP-LE, NF-κB or Dredd, but not in PGRP-LC are rescuing PGRP-LB mutant phenotype. For C, D, E, F and G; shown is the average egg-laying ratio ± SEM from at least two independent trials with at least 20 females per genotype and condition used. * indicates p<0.01; ** indicates p<0.001; n.s. indicates p>0.05, unpaired two-tailed Mann-Whitney test versus indicated controls.