Exploration of the sequential fundamental processes in the early infection stage of Ralstonra solanacearum

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Ralstonia solanacearum first attaches to host plant root surfaces and invades the intercellular spaces of the root cortex. R. solanacearum rapidly multiplies and colonizes within intercellular spaces and vascular parenchyma to finally break into the protoxylem vessels. Plant cell signals are recognized by PrhA on the bacterial outer membrane and transferred to hrpB expression. By using the co-cultivation method of R. solanacearum with Arabidopsis thaliana in the liquid medium, we have investigated the regulation of pathogenicity gene expression, including hrp genes, at these early stages of the infection process. The eps genes responsible for EPS production are known to be induced at the late stage of infection in a cell density-dependent manner by PhcA. While the expression of prhA was constitutive, other genes involved in plant signal cascade and genes in hrp regulon were expressed depending on cell densities. Cell densities of maximal expression for these genes were less than those for eps genes, indicating expression of these genes are repressed after they reach to the maximum. By transposon mutagenesis, PhcA was demonstrated to be a negative regulator of genes in hrp regulon. The expression of phcA itself is known to be activated in a cell density-dependent manner through quorum sensing. Taken all together, we propose the global regulation scheme at early stages of infection involving HrpB and PhcA. After R. solanacearum invades the intercellular spaces, hrpB is induced in response to plant signal and activates hrp regulon, which constructs type III secretion system. R. solanacearum cells can develop with the aid of secreted proteins through the type III system, and cell densities reach to the threshold, in which phcA starts to express. The expressed PhcA represses genes involved in plant signal cascade and hrp regulon, and at the same time activates eps genes and other genes for degradation enzymes.