Axel Kok-Jensen and Peter H. Andersen have no conflicts of interest. “
“The genes in the hrp regulon encode the proteins find more composing type III secretion system in Ralstonia solanacearum. The hrp regulon is positively controlled by HrpB, and hrpB expression is activated by both HrpG and PrhG. We have identified three genes, prhK, prhL, and prhM, which positively control the hrp regulon in strain OE1-1. These genes are likely to form an operon, and this operon is well conserved in the genera Ralstonia and Burkholderia. This indicates that the operon is not specific to the plant pathogens. Mutations in each of these three genes abolished hrpB and prhG expression. prhK, prhL,

and prhM mutant strains lost pathogenicity toward tomato completely, and they were less virulent toward tobacco. PrhK and PrhL share sequence similarity with allophanate hydrolase and PrhM with LamB. This suggests that the three gene products are not transcriptional regulators in the strict sense, but regulate hrp regulon indirectly. This novel class of virulence-related genes will LY294002 mark the beginning of new findings regarding the overall infection mode of R. solanacearum.

Ralstonia solanacearum (Yabuuchi et al., 1995) is a Gram-negative, soil-borne vascular phytopathogen that causes wilt diseases in >200 plant species (Schell, 2000). hrp (hypersensitive response and pathogenicity) genes encode the component proteins of type III secretion system (T3SS) and are essential for the pathogenicity of R. solanacearum (Kanda et al., 2003a). Bacteria use the T3SS to interact with host plants, and to inject virulence factors, the so-called type III effectors, into the host cytosol (Galan & Collmer, 1999). The hrp genes are clustered together and form the hrp regulon (Van Gijsegem et al., 1995). This regulon is repressed in nutrient-rich media (Arlat et al., 1992). Nutrient-poor conditions, which may mimic conditions in the intracellular spaces of plants, induce a 20-fold increase in the expression of hrp regulon (Genin et al., 1992). Plant signals stimulate the expression of operons belonging to the hrp regulon by another Chloroambucil 10–20-fold relative to the expression in nutrient-poor conditions (Marenda

et al., 1998). The hrp regulon is positively regulated by the AraC-type transcriptional regulator HrpB (Genin et al., 1992). Plant signals are perceived by the outer-membrane receptor PrhA, and are transduced to HrpG through PrhR/PrhI and PrhJ (Aldon et al., 2000). HrpG then activates the expression of hrpB (Brito et al., 1999). The HrpG homolog, PrhG, is also a two-component response regulator for the activation of hrpB (Plener et al., 2010). On the other hand, the hrp regulon is negatively regulated by a global virulence regulator, PhcA, in a quorum sensing-dependent manner (Genin et al., 2005). PhcA binds to the promoter region of the prhIR operon, and represses the expression of prhIR. In turn, this shuts down the expression of all downstream genes (Yoshimochi et al., 2009a).