IMD-Pathway Activation Is Downregulated by PGRP-SC1/2

<div><p>(A) Kinetics of <i>diptericin</i> mrna induction <i>(Dipt/RpL32)</i> after infection by various bacteria. Each histogram corresponds to the mean value of five independent experiments (± standard deviation). Asterisks indicate that the difference between <i>DaGal4;UAS iPGRP-SC</i> and control <i>UAS iPGRP-SC</i> values is statistically significant (<i>p <</i> 0.05). One hundred percent corresponds to the level of activation at 6 h in control flies. In the lower panel, <i>diptericin</i> induction after gram-positive bacterial infections were compared to that obtained after infection by E. cloacae (100%). <i>RpL32</i> is used as an internal control. ci, clean injury; ni, noninfected.</p><p>(B) Quantification of <i>diptericin</i> mRNA levels in <i>UAS iPGRP-SA</i>, <i>DaGal4;UAS iPGRP-SA</i> and <i>PGRP-SA^seml</i> flies shows that reduction of <i>PGRP-SA</i> mRNA levels does not influence IMD-pathway induction 6 h after infection by <i>E. coli.</i> Quantification of <i>drosomycin</i> mRNA levels 24 h after M. luteus infection indicates that PGRP-SA is efficiently knocked down by dsRNA interference. <i>PGRP-SA^seml</i> is a complete loss-of-function mutant for PGRP-SA. Each histogram corresponds to the mean value of five independent experiments (± standard deviation). Asterisk indicates that the difference between <i>DaGal4;UAS iPGRP-SA</i> and control <i>UAS iPGRP-SA</i> values is statistically significant (<i>p</i> < 0.05).</p><p>(C) <i>DaGal4;UAS iPGRP-SC</i> flies are as susceptible to infection by E. cloacae as control flies<i>.</i></p><p>(D) E. cloacae and <i>E. coli AmpR</i> growth in various genetic backgrounds 24 h after infection. Flies with reduced levels of PGRP-SC1/2, unlike <i>IKK</i>γ^key1 mutants, are able to clear bacteria from their hemolymph. Each histogram corresponds to the mean value of four independent experiments (± standard deviation).</p>