Figure 2. One specific PGRP-LB isoform controls oviposition.

(A) PGRP-LB locus organization. Three PGRP-LB isoforms are produced from the locus. The green lines represent the cloned fragments used to generate the Gal4 constructs. (B) Egg-laying ratio of PGRP-LB females carrying various Gal4 drivers (pLB1^Gal4, pLB2 ^Gal4, pLB3 ^Gal4) and UAS constructs allowing the overexpression of the three different PGRP-LB isoforms (PGRP-LB^PA, PGRP-LB^PC, PGRP-LB^PD). A single Gal4-UAS combination (pLB1^Gal4/UAS–PGRP-LB^PD) is rescuing the egg-laying drop seen in infected PGRP-LB mutant females. (C) Egg-laying ratio of PGRP-LB mutant females and CRISPR-Cas9-generated PGRP-LB^PD only mutants. For B and C: 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 wt animals.

DOI: http://dx.doi.org/10.7554/eLife.21937.007

Figure 2—figure supplement 1. While all PGRP-LB isoforms possess amidase activity, PGRP-LB^PD isoform is not required for the negative regulation of the systemic immune response.

(A) Quantification of Diptericin mRNA in wt and PGRP-LB mutant guts expressing the different PGRP-LB isoforms under the control of the gut specific Gal4 driver, NP1^Gal4 and orally infected with Ecc15. (B) Amino acid sequence alignment showing the deletions in the PGRP-LB^PD isoform-specific mutants generated. In bold are the amino acids specific of the PGRP-LB^PD isoform. (C) Quantification of Diptericin mRNA in wt, PGRP-LB mutant and PGRP-LB^PD isoform-specific mutants fat body orally infected with Ecc15.

DOI: http://dx.doi.org/10.7554/eLife.21937.008