YopK contributes to caspase-3 cleavage through the extrinsic pathway.

<p>A) RAW 264.7 macrophages were infected with KIM5, KIM5 <i>yopJ</i>C172A, or KIM6⁻ at an MOI of 20 and assayed for caspase-3 activity after 3.5 hours of infection. Data shown are the mean of four biological replicates, collected in two independent trials, and are shown as a percentage of caspase-3 activity from WT-infected cells. B–D) RAW 264.7 macrophages were left untreated (white bars) or treated with inhibitors (grey bars) for (B) caspase-9 (Z-LEHD-FMK), (C) caspase-8 (IETD), or (D) JNK (SP600125) and infected with either <i>Y. pestis</i> KIM D27 or KIM D27 <i>yopK</i> at an MOI of 20. After 3.5 hours of infection, cell pellets were analyzed for cleaved caspase-3. Data shown are the mean of four replicates, collected in two independent trials and are shown as percent of untreated for each strain. Statistical significance by one-way ANOVA followed by Tukey post-hoc test, *<i>p</i><0.05, ns not significant.