ArticlePLoS pathogens2006
Legionella pneumophila exploits PI(4)P to anchor secreted effector proteins to the replicative vacuole.
Article in PLoS pathogens, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers.
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Who cites it
155 citing papers in PubMed.
- The Legionella effector RidL binds the large fission GTPase Drp1 to promote mitochondrial fragmentation.EMBO reports · 2026Article
- Localization of the PelC and PelE effectors to theInfection and immunity · 2026Article
- Regulation of ribosome hibernation controlsmBio · 2026Article
- Molecular evolution and adaptations ofFrontiers in cellular and infection microbiology · 2026Review
- Overexpression ofPlant signaling & behavior · 2025Article
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- Bacterial pathogens hijack host cell peroxisomes for replication vacuole expansion and integrity.Science advances · 2025Article
- Inter-kingdom signaling by the Legionella autoinducer LAI-1 involves the antimicrobial guanylate binding protein GBP.PLoS pathogens · 2025Article
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- The hidden dancers in water: the symbiotic mystery ofFrontiers in microbiology · 2025Review
- Small molecule communication ofMicrobiology and molecular biology reviews : MMBR · 2024Review
- Review
- Cross-family small GTPase ubiquitination by the intracellular pathogenMolecular biology of the cell · 2024Article
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- Ubiquitin-targeted bacterial effectors: rule breakers of the ubiquitin system.The EMBO journal · 2023Review
- Article
- Legionella- and host-driven lipid flux at LCV-ER membrane contact sites promotes vacuole remodeling.EMBO reports · 2023Article
- Cellular cholesterol licensesMicrobial cell (Graz, Austria) · 2023Article
- Review
- Imaging Flow Cytometry of Legionella-Containing Vacuoles in Intact and Homogenized Wild-Type and Mutant Dictyostelium.Methods in molecular biology (Clifton, N.J.) · 2023Article
95 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
The causative agent of Legionnaires' disease, Legionella pneumophila, employs the intracellular multiplication (Icm)/defective organelle trafficking (Dot) type IV secretion system (T4SS) to upregulate phagocytosis and to establish a replicative vacuole in amoebae and macrophages. Legionella-containing vacuoles (LCVs) do not fuse with endosomes but recruit early secretory vesicles. Here we analyze the role of host cell phosphoinositide (PI) metabolism during uptake and intracellular replication of L. pneumophila. Genetic and pharmacological evidence suggests that class I phosphatidylinositol(3) kinases (PI3Ks) are dispensable for phagocytosis of wild-type L. pneumophila but inhibit intracellular replication of the bacteria and participate in the modulation of the LCV. Uptake and degradation of an icmT mutant strain lacking a functional Icm/Dot transporter was promoted by PI3Ks. We identified Icm/Dot-secreted proteins which specifically bind to phosphatidylinositol(4) phosphate (PI(4)P) in vitro and preferentially localize to LCVs in the absence of functional PI3Ks. PI(4)P was found to be present on LCVs using as a probe either an antibody against PI(4)P or the PH domain of the PI(4)P-binding protein FAPP1 (phosphatidylinositol(4) phosphate adaptor protein-1). Moreover, the presence of PI(4)P on LCVs required a functional Icm/Dot T4SS. Our results indicate that L. pneumophila modulates host cell PI metabolism and exploits the Golgi lipid second messenger PI(4)P to anchor secreted effector proteins to the LCV.
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