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Genetic screening of Hrp type III‐related pathogenicity genes controlled by the HrpB transcriptional activator in Ralstonia solanacearum
Author(s) -
Mukaihara Takafumi,
Tamura Naoyuki,
Murata Yukio,
Iwabuchi Masaki
Publication year - 2004
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2004.04328.x
Subject(s) - biology , ralstonia solanacearum , gene , gene cluster , effector , genetics , mutant , escherichia coli , operon , transposable element , microbiology and biotechnology , bacteria , biochemistry
Summary As in many other Gram‐negative phytopathogenic bacteria, the Hrp type III secretion system is essential for the pathogenicity of Ralstonia solanacearum on host plants. The expression of most of the type III effector genes previously isolated from R. solanacearum is co‐regulated with those of hrp genes by an AraC‐type transcriptional activator, HrpB. In order to isolate type III‐related pathogenicity genes, we screened hrpB ‐regulated genes in R. solanacearum . Using a transposon‐based system, we isolated 30 novel hpx ( h r p B ‐dependent e x pression) genes outside the hrp gene cluster. Most of the hpx genes contain a PIP ( p lant‐ i nducible p romoter) box‐like motif in their putative promoter regions. Seven hpx genes encoded homologues of known type III effectors and type III‐related proteins found in other animal and plant pathogens. Four encoded known enzymes, namely, glyoxalase I, Nudix hydrolase, spermidine synthase and transposase. Interestingly, six hpx genes encoded two types of leucine‐rich repeat (LRR) protein. Products of the remaining genes did not show any significant homology to known proteins. We also identified two novel hrpB ‐regulated genes, hpaZ and hpaB , downstream of hrpY in the hrp cluster. The hpaB gene of R. solanacearum , but not hpaZ , was required for both the pathogenicity and ability to induce hypersensitive reaction on plants. We show that a hpaB null mutant still produces Hrp pili on the cell surface although it shows a typical Hrp‐defective phenotype on plants.