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- W1267541968 abstract "To test whether the phenotype of the pilD mutant is due to loss of the type II protein secretion system and/or the type IV pilus assembly apparatus, the authors employed a genetic approach. First, the authors mutated two loci involved in type II protein secretion. Second, the authors analyzed the phenotypes of two mutants defective in the biogenesis of Legionella pneumophila type IV pilus. The protease, acid phosphatase, and pnitrophenyl phosphorylcholine (PNPPC) hydrolase activities were similarly reduced in the supernatant of the pilD, lspDE, and lspG mutants compared with the wild type and the pilEL and pilQ mutant strains. In addition, the lipase and phospholipase A activities were also reduced in the supernatants of both Isp mutants relative to the wild type and the pilEL mutant. These results demonstrate that five pilD-dependent activities are secreted by the L. pneumophila type II protein secretion pathway. Indeed, the small growth defect exhibited by some pilQ mutants in U937 cells could hint at a minor role of the type IV pilus assembly apparatus itself for macrophage infection. This defect, added to the small defect due to the loss of type II secretion, could account for the growth impairment of the pilD mutant in macrophages. Alternatively, PilD could control a third unidentified pathway promoting macrophage infection. Thus, continued analysis of L. pneumophilapilD, lsp, and pilus mutants should not only expand our understanding of Legionnaires’ disease but may provide new paradigms for protein secretion systems." @default.
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- W1267541968 date "2014-04-30" @default.
- W1267541968 modified "2023-09-26" @default.
- W1267541968 title "Role of the Type II Protein Secretion Pathway in Pathogenesis of Legionella pneumophila" @default.
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- W1267541968 doi "https://doi.org/10.1128/9781555817985.ch2" @default.
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