ArticleInfection and immunity2014
The Legionella longbeachae Icm/Dot substrate SidC selectively binds phosphatidylinositol 4-phosphate with nanomolar affinity and promotes pathogen vacuole-endoplasmic reticulum interactions.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 63 citations in OpenAlex.
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- Probing and imaging phospholipid dynamics in live cells.Life metabolism · 2024Review
- Recombinant biosensors for multiplex and super-resolution imaging of phosphoinositides.The Journal of cell biology · 2024Article
- Legionella- and host-driven lipid flux at LCV-ER membrane contact sites promotes vacuole remodeling.EMBO reports · 2023Article
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- Legionella longbeachae effector protein RavZ inhibits autophagy and regulates phagosome ubiquitination during infection.PloS one · 2023Article
- Type II phosphatidylinositol 4-kinases function sequentially in cargo delivery from early endosomes to melanosomes.The Journal of cell biology · 2022Article
- An update on genetically encoded lipid biosensors.Molecular biology of the cell · 2022Article
- TheCurrent research in microbial sciences · 2022Article
- Evolution and Adaptation ofBiomolecules · 2021Review
- Monitoring Phosphoinositide Fluxes and Effectors During Leukocyte Chemotaxis and Phagocytosis.Frontiers in cell and developmental biology · 2021Review
- Divergence of Legionella Effectors Reversing Conventional and Unconventional Ubiquitination.Frontiers in cellular and infection microbiology · 2020Review
- Phosphoinositides and the Fate ofFrontiers in immunology · 2020Review
- SopF, a phosphoinositide binding effector, promotes the stability of the nascent Salmonella-containing vacuole.PLoS pathogens · 2019Article
- Study ofInfection and immunity · 2019Article
- PIKfyve/Fab1 is required for efficient V-ATPase and hydrolase delivery to phagosomes, phagosomal killing, and restriction of Legionella infection.PLoS pathogens · 2019Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Legionella spp. cause the severe pneumonia Legionnaires' disease. The environmental bacteria replicate intracellularly in free-living amoebae and human alveolar macrophages within a distinct, endoplasmic reticulum (ER)-derived compartment termed the Legionella-containing vacuole (LCV). LCV formation requires the bacterial Icm/Dot type IV secretion system (T4SS) that translocates into host cells a plethora of different "effector" proteins, some of which anchor to the pathogen vacuole by binding to phosphoinositide (PI) lipids. Here, we identified by unbiased pulldown assays in Legionella longbeachae lysates a 111-kDa SidC homologue as the major phosphatidylinositol 4-phosphate [PtdIns(4)P]-binding protein. The PI-binding domain was mapped to a 20-kDa P4C [PtdIns(4)P binding of SidC] fragment. Isothermal titration calorimetry revealed that SidC of L. longbeachae (SidC(Llo)) binds PtdIns(4)P with a K(d) (dissociation constant) of 71 nM, which is 3 to 4 times lower than that of the SidC orthologue of Legionella pneumophila (SidC(Lpn)). Upon infection of RAW 264.7 macrophages with L. longbeachae, endogenous SidC(Llo) or ectopically produced SidC(Lpn) localized in an Icm/Dot-dependent manner to the PtdIns(4)P-positive LCVs. An L. longbeachae ΔsidC deletion mutant was impaired for calnexin recruitment to LCVs in Dictyostelium discoideum amoebae and outcompeted by wild-type bacteria in Acanthamoeba castellanii. Calnexin recruitment was restored by SidC(Llo) or its orthologues SidC(Lpn) and SdcA(Lpn). Conversely, calnexin recruitment was restored by SidC(Llo) in L. pneumophila lacking sidC and sdcA. Together, biochemical, genetic, and cell biological data indicate that SidC(Llo) is an L. longbeachae effector that binds through a P4C domain with high affinity to PtdIns(4)P on LCVs, promotes ER recruitment to the LCV, and thus plays a role in pathogen-host interactions.
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