ArticleCellular microbiology2009
Large-scale identification of Legionella pneumophila Dot/Icm substrates that modulate host cell vesicle trafficking pathways.
Article in Cellular microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 157 citations in OpenAlex.
- Genomic divergence and phenotypic heterogeneity ofApplied and environmental microbiology · 2026Article
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- A random mutagenesis screen enriched for missense mutations in bacterial effector proteins.G3 (Bethesda, Md.) · 2024Article
- Genetic evidence for a regulated cysteine protease catalytic triad in LegA7, abioRxiv : the preprint server for biology · 2024Article
- Structural basis for the toxicity of Legionella pneumophila effector SidH.Nature communications · 2023Article
- Eat or Be Eaten: Strategies Used byInfection and immunity · 2023Review
- Rapid adaptations ofMicrobial genomics · 2023Article
- VpdC is a ubiquitin-activated phospholipase effector that regulatesProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Glycosylating Effectors ofBiomolecules · 2022Review
- Knowledge to Predict Pathogens:Microorganisms · 2022Review
- Pathogenicity and Virulence ofVirulence · 2021Review
- Quorum sensing governs a transmissive Legionella subpopulation at the pathogen vacuole periphery.EMBO reports · 2021Article
- Major Outer Membrane Protein fromJournal of immunology research · 2021Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The bacterial pathogen Legionella pneumophila replicates in a specialized vacuole within host cells. Establishment of the replication vacuole depends on the Dot/Icm translocation system that delivers a large number of protein substrates into the host cell. The functions of most substrates are unknown. Here, we analysed a defined set of 127 confirmed or candidate Dot/Icm substrates for their effect on host cell processes using yeast as a model system. Expression of 79 candidates caused significant yeast growth defects, indicating that these proteins impact essential host cell pathways. Notably, a group of 21 candidates interfered with the trafficking of secretory proteins to the yeast vacuole. Three candidates that caused yeast secretory defects (SetA, Ceg19 and Ceg9) were investigated further. These proteins impinged upon vesicle trafficking at distinct stages and had signals that allowed translocation into host cells by the Dot/Icm system. Ectopically produced SetA, Ceg19 and Ceg9 localized to secretory organelles in mammalian cells, consistent with a role for these proteins in modulating host cell vesicle trafficking. Interestingly, the ability of SetA to cause yeast phenotypes was dependent upon a functional glycosyltransferase domain. We hypothesize that SetA may glycosylate a component of the host cell vesicle trafficking machinery during L. pneumophila infection.
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