Skip to main content
. 2019 Feb 26;8:e44341. doi: 10.7554/eLife.44341

Figure 6. Identification of AMPs involved in the susceptibility of ΔAMPs flies to E.cloacae.

(A) Survival of mutants for groups of AMPs reveals that loss of Imd-responsive Group B peptides (Drosocin, Attacins, and Diptericins) results in a strong susceptibility to infection (p<0.001), while loss of Group A or C peptides alone resists as wild-type (p>0.1 each). Group AB flies were as susceptible as ΔAMPs flies, and we observed a synergistic interaction between Group A and B mutations (A*B: HR =+2.55, p=0.003). (B) Further dissection of the mutations in Group B revealed that loss of Drosocin alone (DroSK4), or a deficiency lacking both Drosocin and Attacins AttA and AttB (Dro-AttABSK2) recapitulates the susceptibility of Group B flies. (C) By 18hpi, bacterial loads in individual Drosocin mutants or RelE20 flies are significantly higher than wild-type. (D) Heterozygote flies for DroSK4 and Df(2R)BSC858 (a deficiency removing Drosocin, Attacins AttA and AttB, and other genes) are strongly susceptible to E. cloacae infection. (E) Drosocin mutants in an alternate genetic background (yw) are susceptible to E. cloacae. One-way ANOVA: not significant = ns, and p<0.001 = *** relative to iso w1118.

Figure 6.

Figure 6—figure supplement 1. Additional validation of the role of Drosocin in defence against E. cloacae.

Figure 6—figure supplement 1.

(A) Drosocin mutant susceptibility remains even at a lower dose (OD = 10,~7000 bacteria/fly), while RelE20 flies succumb rapidly regardless of initial dose. (B) Silencing of Drosocin by RNAi leads to significant mortality from E. cloacae infection (p<0.001). (C) Validation of the Drosocin RNAi construct 6hpi.