FIG 4.

KV induction and suppression of NF-ΚB pathways are mediated by gp83. The ability of KV to inhibit Toll (A), induce Imd (B), and inhibit JAK-STAT (C) was assessed during gp83 knockdown, using two independent dsRNAs against gp83 (labeled ds-gp83²⁰⁰ and ds-gp83⁵⁸³). Drosomycin, diptericin, and 10×STAT activities were measured as Drs-FLuc, Dpt-FLuc, and 10×STAT-FLuc expression, relative to RLuc expression as described in the legend to Fig. 3. For each, data are presented as fold change in signalling following KV infection relative to mock infection (chloroform-treated KV) (4 dpi), where 1 (horizontal dotted line) represents no induction or suppression of the pathway by KV infection. (A) Fold change in Drs-FLuc expression following KV infection of S2 cells with (orange bars) or without (gray bars) activation of the pathway by Toll^LRR expression. (B) Fold change in Dpt-FLuc expression following KV infection of S2 cells with (orange bars) or without (gray bars) pathway activation by PGRP-LC expression. (C) Fold change in 10×STAT FLuc expression following KV infection of S2 cells. (D) Efficiency of gp83 knockdown was assessed by cotransfection of an expression plasmid encoding gp83 with two independent dsRNAs against gp83 and Drs-FLuc reporter plasmids. Error bars show SEMs (n = 5 biological replicates for panels A to C and n = 3 biological replicates for panel D).