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. 2008 Dec 1;77(2):860–866. doi: 10.1128/IAI.00995-08

FIG. 3.

FIG. 3.

GAG-binding activity of ACP promotes GBS virulence. (A) The products of Drosophila genes ttv and DEXT2 (sotv) form a heterodimeric GAG-polymerizing complex. We generated heterozygous ttv DEXT2 (sotv) mutants by crossing strain FRTG13 ttv00681 sotv 1.8.1/CyO with wild-type strain OreR. The Kaplan-Meier survival plot reveals that these mutants resisted lethal infection with wild-type GBS strain A909 more effectively than did wild-type OreR flies (P < 0.001). (B) We crossed mutant lines with OreR to generate flies with heterozygous mutations in the HSPGs sdc and dally, as well as flies with mutations in both dally and dally-like protein and in sdc, dally, and dally-like protein. All mutants resisted infection with A909 compared to wild-type OreR flies (P, <0.001 versus wild-type results). (C) A charge-neutralizing mutation in GBS strain A909/R185A impairs ACP-GAG binding. The Kaplan-Meier survival plot shows longer survival after fly infection with the mutant than after that with wild-type A909 (median survival times, 26.5 ± 0.04 h for A909 infection versus 48 ± 0.04 h for A909/R185A infection [P < 0.001; log-rank test]). Results for the sterile THB-injected control sample are shown. Plots show results from at least 70 flies per sample.