Figure 6.

Model for virulence gene and regulator acquisition in X. cannabis. The acquisition of various virulence traits was likely sequential in Xanthomonas spp., which represented by a schematic phylogenetic tree. Cell-wall modification by cell-wall degrading enzymes (CWDEs) is an ancient trait found in both Xylella and Xanthomonas, which suggests their acquisition predates the separation of these two pathogenic genera. Genes encoding the regulators HpaR2 and HpaS were subsequently acquired before the separation of the Xanthomonas Group 2 and early branching Group 1. Then the regulatory genes hrpX and hrpG were gained by Group 2 strains and further promoters (e.g., PIP boxes) evolved to adapt to these virulence regulators. This is further supported by the absence of PIP boxes in front of non-hrp genes in Group 1 strains (X. albilineans and X. sacchari). Because the organization of hrpX and hrpG and the T3SS is more similar to R. solanacearum, different than Group 2 xanthomonads and lacking in most Group 1 species (X. sacchari and X. albilineans), we suspect an independent acquisition of this system in X. translucens. hrpG and hrpX are present in a similar location in all sequenced Group 2 species. We hypothesize that the T3SS and core effectors were either (1) acquired independently by individual pathovars or (2) acquired an earlier point and lost in some pathovars. After the acquisiton of the T3SS, we posit that accessory effectors were acquired (3) by horizontal gene transfer to alter host range and/or promote susceptibility by suppressing plant immunity.