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The Hrp Cluster Of Pseudomonas Syringae: APathogenicity Island Encoding A Type III Protein Translocation Complex?
Published 1999 · Biology
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This chapter focuses on the pathogenicity determinants of Pseudomonas syringae as a paradigm for microbial pathogenesis in plants. It focuses specifically upon genetic determinants of P. syringae strains necessary for colonization of plant tissue. As in mammalian pathogens, essential pathogenicity determinants of several plant-pathogenic bacteria are localized in apparent pathogenicity islands (PAIs). Proteins translocated by a type III protein translocation complex (PTC) similar to that of its mammalian counterparts mediate both the pathogenicity and host range of P. syringae strains. Hybridization analysis indicates that all P. syringae strains carry a homolog to HrpW and that a homolog is present in the closely related Erwinia hrp cluster. The pectate lyase-like domain was the most highly conserved region of the protein from two P. syringae strains. The genetic organization of clusters and regulatory mechanisms controlling environmental regulation are clearly distinct between the two groups of hrp clusters. For example, the primary regulatory factor for the X. campestris and R. solanacearum hrp clusters is an AraC homolog (HrpX and HrpB, respectively. By analogy to mammalian pathogens, pathogenesis by plant pathogenic bacteria, such as P. syringae, probably involves (i) adhesion of the bacteria to plant cells, (ii) activation of a type III PTC, (iii) translocation of pathogenicity determinants into plant cells, (iv) physiological changes in the host cells to stimulate the release of nutrients, (v) production of virulence factors to facilitate the growth of the bacteria, and (vi) growth and spread of the bacteria to surrounding cells in the tissue.
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