The XopE2 effector protein of Xanthomonas campestris pv. vesicatoria is involved in virulence and in the suppression of the hypersensitive response

Abstract

Pathogenicity of Xanthomonas campestris pv. vesicatoria (Xcv) causing bacterial spot disease on tomato (Lycopersicon spp.) and pepper (Capsicum spp.) requires the type III secretion system (T3SS) and T3SS effectors. In this study, we employed the AFLP technique to investigate the diversity of X campestris pv. vesicatoria isolated in Taiwan, and consequently a XopE2 homologue was identified in all fourteen Xcv strains that have been classified into two groups. Phylogenic analysis of XopE2 amino acid sequences indicated that XopE2 of Xcv Xvt122 (group A) has a closer genetic distance to XopE2 of Xcv 85-10 than to that of Xcv Xvt45 (group B). Interestingly, although it was suggested that Xvt45 contains duplicated xopE2 genes, one being located on the genome and the other located on a large plasmid, a single copy deletion of xopE2 within the gnome caused a substantial reduction in virulence, but no effect of xopE2 mutation on virulence of Xcv 85-10 and Xvt122 was observed. Furthermore, our results revealed that XopE2 of Xcv Xvt122 or Xcv Xvt45 was able to suppress HR in a T3SS-dependent manner and the heterologously-expressed XopE2 was sufficient to modulate the virulence on susceptible tomato plants. Their biological functions are not dependent on the consensus catalytic triad (159(th) cysteine) and thiol-protease His residue (47(th) histidine) of XopE2.