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. 2017 Jan 13;13(1):e1006569. doi: 10.1371/journal.pgen.1006569

Fig 3. AMP expression in infected PGRP-LF mutants.

Fig 3

(A) Overexpression of AttacinD and Diptericin mRNAs in PGRP-LF mutant larvae (either PGRP-LFKO or PGRP-LFKO/Df(3L)BSC113) requires a functional PGRP-LC/IMD cascade. Inactivation of IMD, Dredd, Diap2 and Relish, but not dMyd88 or PGRP-LE, completely suppresses both AttacinD and Diptericin ectopic expression in PGRP-LF mutants. Expression of UAS-PGRP-LF under the control of PGRP-LFGal4strong suppresses the ectopic expression of AMPs observed in PGRP-LF mutants (B) Ectopic activation of AMP is not detected in mutants for other IMD pathway negative regulators such as Pirk or PGRP-LB. (C) IMD pathway activation, monitored by Diptericin expression, 5h after septic infection with Ecc. Although Diptericin is constitutively expressed at higher levels in uninfected PGRP-LF mutants (PGRP-LFKO/Df(3L)BSC113) than in wild-type, Diptericin mRNA levels are similar in fat body of wild-type and PGRP-LF mutant flies infected by septic injury. (D) IMD pathway activation, monitored by Diptericin expression, 24h after Ecc oral infection. While PGRP-LF inactivation does not modify IMD pathway inducibility in the midgut of Ecc orally infected flies, it does so in the fat body. For (A), (B), (C) and (D) mRNA level in controls was set to 1, and values obtained with indicated genotypes were expressed as a fold of this value. For (A) (B) (C) and (D) histograms correspond to the mean value ± SD of three independent experiments. Values indicated by symbols (*) are statistically significant (t-test, p < 0.05). ns: not significantly different.