. "Pseudomonas syringae Hrp Type III Secretion System and Effector Proteins." (NAS Colloquium) Virulence and Defense in Host--Pathogen Interactions: Common Features Between Plants and Animals. Washington, DC: The National Academies Press, 2001.
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COLLOQUIUM ON Virulence and Defense in Host—Pathogen Interactions: Common Features Between Plants and Animals
secreted across inner and outer membranes by machinery that is common to all type III systems. However, translocation into host cells is likely to be unique because of adaptations to the fundamentally different surfaces of plant and animal cells.
Our investigation of the basis for P. syringae phytopathogenicity has focused on the mechanisms underlying elicitation of the HR, a signature of plant encounters with incompatible phytopathogens, and it has revealed the modular nature of the process and its underlying genetics. Thus, the requirements for HR elicitation can be reduced to two components: a functional Hrp type III secretion system and an injected effector protein that is recognized by the R-gene surveillance system of the test plant. Hrp protein secretion in culture can be further dissected genetically, revealing two operons directing export across the inner membrane and another directing export across the outer membrane. The effector proteins also appear modular in their possession of a universal type III targeting signal in the 5′ ends of their cognate mRNAs. This modularity has several experimental consequences: a cloned P. syringae Hrp system is sufficient to direct heterologous secretion and delivery of effector proteins by nonphytopathogenic bacteria; effector proteins from P. syringae can be heterologously delivered into plants by Erwinia Hrp systems or secreted in culture by the Yersinia type III system; and the need for any Hrp system for HR elicitation can be circumvented entirely by delivery of effector protein genes into plant cells by biolistics or Agrobacterium-mediated transformation. The modular nature of the Hrp/effector system is also seen in the tripartite mosaic architecture of the P. syringae Hrp Pai, which features both exchangeable and conserved effector loci. The EEL represents a region in flux because of its high frequency of recombination, and this probably allows fine tuning of pathogenicity. On the basis of its similar G + C content to the hrp/hrc cluster and the rest of the P. syringae chromosome, the CEL was probably acquired at the same time as the core hrp/hrc cluster, and it encodes effectors that contribute more significantly to pathogenicity than the EEL. The modular nature of the Hrp/effector system suggests that it functions universally in a broad range of potential plant hosts and with a frequently changing pool of effectors. Effector gene instability may be driven by the evolution of R gene surveillance systems and changes in effector targets in plants. The next challenge is to identify all of the effector proteins produced by model strains of P. syringae, to understand how these proteins promote parasitism, and to understand how the type III system of phytopathogens has been adapted to deliver these proteins across plant cell walls.
We thank Nam-Hai Chua (The Rockefeller University, New York, NY) for providing pTA7002. This work was supported by National Science Foundation grant MCB 97–35303-4488 (A.C.), National Research Initiative Competitive Grants Program United States Department of Agriculture grants 98–35303-6464 (J.R.A.) and 98–35303-6662 (D.E.F.), and United States Public Health Service Grant AI 42797 from the National Institutes of Health—National Institute of Allergy and Infectious Diseases Branch (O.S.).
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