Initial evidence on auto-regulation of prhK operon and its potential working model for the regulation of hrp regulon in Ralstonia solanacearum

Ralstonia solanacearum is a causative agent of bacterial wilt in many plant species and has been studied as a model plant vascular pathogen. hrp regulon and its encoding type III secretion system are responsible for the pathogenicity of R. solanacearum on host plants. Transcriptional regulator HrpB controls hrp regulon, and both HrpG and PrhG regulate hrpB expression. PrhA-PrhR/I-PrhJ-HrpG signal cascade activates hrpB expression. While PrhG is independent of this cascade, it is activated by prhk, prhL and prhM, which form one operon. Each of these three genes is essential for the pathogenicity of R. solanacearum on host plants, but their products are not transcriptional regulators. They are well conserved in Betaproteobacteria and control some other virulence related genes rather than PrhG and hrp regulon. here, after evaluating the regulation between the se three genes and some known virulence genes, we provide some initial evidence on the autoregulation of this operon and proposed the potential working model of prhK operon on hrp regulon in R. solanacearum.