ArticleJournal of bacteriology2013
Refining the plasmid-encoded type IV secretion system substrate repertoire of Coxiella burnetii.
Article in Journal of bacteriology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed.
- Review
- Comparative Transcriptomics and Genomics from Continuous Axenic Media Growth IdentifiesbioRxiv : the preprint server for biology · 2023Article
- Genomic detection ofVeterinary research forum : an international quarterly journal · 2023Article
- The endogenous Coxiella burnetii plasmid encodes a functional toxin-antitoxin system.Molecular microbiology · 2022Article
- Characterization ofMicroorganisms · 2022Article
- Developmental Transitions Coordinate Assembly of the Coxiella burnetii Dot/Icm Type IV Secretion System.Infection and immunity · 2022Article
- A protein-protein interaction map reveals that the Coxiella burnetii effector CirB inhibits host proteasome activity.PLoS pathogens · 2022Article
- To die or not to die: Programmed cell death responses and their interactions with Coxiella burnetii infection.Molecular microbiology · 2022Article
- Coxiella burnetii and Related Tick Endosymbionts Evolved from Pathogenic Ancestors.Genome biology and evolution · 2021Article
- TheJournal of bacteriology · 2021Article
- Article
- Coxiella burnetii: international pathogen of mystery.Microbes and infection · 2020Review
- Interfering with Autophagy: The Opposing Strategies Deployed byFrontiers in cellular and infection microbiology · 2020Review
- Comparative virulence of diverse Coxiella burnetii strains.Virulence · 2019Article
- Prediction of T4SS Effector Proteins forFrontiers in microbiology · 2019Article
- The Effector Cig57 Hijacks FCHO-Mediated Vesicular Trafficking to Facilitate Intracellular Replication of Coxiella burnetii.PLoS pathogens · 2016Article
- The Type IV Secretion System Effector Protein CirA Stimulates the GTPase Activity of RhoA and Is Required for Virulence in a Mouse Model of Coxiella burnetii Infection.Infection and immunity · 2016Article
- Right on Q: genetics begin to unravel Coxiella burnetii host cell interactions.Future microbiology · 2016Review
- Article
- Dining in: intracellular bacterial pathogen interplay with autophagy.Current opinion in microbiology · 2016Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
The intracellular bacterial agent of Q fever, Coxiella burnetii, translocates effector proteins into its host cell cytosol via a Dot/Icm type IV secretion system (T4SS). The T4SS is essential for parasitophorous vacuole formation, intracellular replication, and inhibition of host cell death, but the effectors mediating these events remain largely undefined. Six Dot/Icm substrate-encoding genes were recently discovered on the C. burnetii cryptic QpH1 plasmid, three of which are conserved among all C. burnetii isolates, suggesting that they are critical for conserved pathogen functions. However, the remaining hypothetical proteins encoded by plasmid genes have not been assessed for their potential as T4SS substrates. In the current study, we further defined the T4SS effector repertoire encoded by the C. burnetii QpH1, QpRS, and QpDG plasmids that were originally isolated from acute-disease, chronic-disease, and severely attenuated isolates, respectively. Hypothetical proteins, including those specific to QpRS or QpDG, were screened for translocation using the well-established Legionella pneumophila T4SS secretion model. In total, six novel plasmid-encoded proteins were translocated into macrophage-like cells by the Dot/Icm T4SS. Four newly identified effectors are encoded by genes present only on the QpDG plasmid from severely attenuated Dugway isolates, suggesting that the presence of specific effectors correlates with decreased virulence. These results further support the idea of a critical role for extrachromosomal elements in C. burnetii pathogenesis.
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