|Hirano, Susan - UNIVERSITY OF WISCONSIN|
|Charkowski, Amy - CORNELL UNIVERSITY|
|Collmer, Alan - CORNELL UNIVERSITY|
Submitted to: Proceedings of the National Academy of Sciences
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 10, 1999
Publication Date: N/A
Interpretive Summary: Many bacterial genes have been identified that are required for the bacteria to be able to cause disease. These genes are of interest because by studying them we can better understand the way that bacteria cause disease. One problem often encountered is that strains lacking such genes often have lost more than one function, that is, they are said to be pleiotropic. A group of genes, known as hrp genes, are required for pathogenicity in the bacterium Pseudomonas syringae pv. syringae (Pss) and other plant pathogenic bacteria. These genes also are required for growth of these bacteria in association with the plants. An important question that had not been resolved was whether the inability of the bacteria to cause disease was associated with their inability to grow, or whether the bacteria had lost both the ability to grow in association with plants and the ability to cause disease. We studied mutants lacking certain hrp genes in field and laboratory experiments. Conditions under which the bacteria would grow in association with plants were identified. When large population sizes of the mutant bacteria grew in association with leaves, lesions were found on those leaves. The disease was caused by the mutants. Thus, the inability of hrp mutants to cause disease is attributable to the inability of these mutants to grow in association with plants. This entirely new finding is important because it will lead scientists in a new direction in their search for mechanisms of disease causation and prevention.
Technical Abstract: The hrp genes have been reported to be required for pathogenicity in Pseudomonas syringae pv. syringae (Pss) and other phytopathogenic bacterial species. A subset of these genes encode a type III secretion system through which virulence factors are thought to be delivered to plant cells.In this study, we sought to better understand the role that hrp pgenes play in interactions of Pss with its host as they occur naturally under field conditions. Population sizes of hrp mutants with defects in genes which encode components of the Hrp secretion system (hrcC::nptII and hrpJ::Spc) and a protein secreted via the system (hrpZ::nptII) were similar to wild type Pss B728a on germinating seeds. However, phyllosphere (i.e., leaf) population sizes of the hrcC and hrpJ secretion mutants, but not the hrpZ mutant, were significantly reduced relative to wild type. Thus, the Hrp type III secretion system, but not HrpZ, plays an important role in enabling Pss to flourish in the phyllosphere, but not the spermosphere. The hrcC and hrpJ mutants caused brown spot lesions at a low frequency when they were inoculated onto seeds at the time of planting. Pathogenic reactions were also found when the hrp secretion mutants were co-infiltrated into bean leaves with a non-lesion forming gacS mutant of B728a. In both cases, the occurrence of disease was associated with elevated population sizes of the hrp secretion mutants. On the basis of the results obtained, it appears that the role of the Hrp type III secretion in pathogenicity is mediated by its requirement in enabling Pss to grow in the phyllosphere.