Fig. 6.

Icm/Dot-dependent translocation of C. burnetii effectors identified by the HSMM and their expression during infection. (A) WT strain JR32 (gray bars) and the icmT deletion mutant GS3011 (white bars) harboring the CyaA fusion proteins (indicated below each bar) were used to infect HL-60–derived human macrophages, and the cAMP levels of the infected cells were determined as described in Materials and Methods. V, vector control. The bar heights represent the means of the amount of cAMP per well obtained in at least three independent experiments; error bars indicate SDs. The cAMP levels of each fusion were found to be significantly different (*P < 0.05; **P < 0.01; ***P < 0.001, paired Student t test) between the WT strain and the icmT deletion mutant. (B) Gene expression levels of C. burnetii effector genes during growth in ACCM-2 axenic medium and in HEK 293T cells. The heat map shows the logarithm of expression values of specific genes during growth in ACCM-2 media or in HEK 293T cells. Four genes were used as controls: dotA and rpoB, as well as coxDFB1 and cbu2056, two previously identified effectors. The values are the RNA levels normalized to 16S RNA during exponential (E) and postexponential (PE) phases. The RNA levels were measured by RT-qPCR and normalized to the levels of 16S RNA as described in Materials and Methods.