ArticlePloS one2012
Identification of a novel small RNA modulating Francisella tularensis pathogenicity.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Ribosome heterogeneity results in leader sequence-mediated regulation of protein synthesis inJournal of bacteriology · 2023Article
- Complement Receptor 3-Mediated Inhibition of Inflammasome Priming by Ras GTPase-Activating Protein DuringFrontiers in immunology · 2018Article
- Whole genome transcriptomics reveals global effects including up-regulation of Francisella pathogenicity island gene expression during active stringent response in the highly virulent Francisella tularensis subsp. tularensis SCHU S4.Microbiology (Reading, England) · 2017Article
- Use of siRNA molecular beacons to detect and attenuate mycobacterial infection in macrophages.World journal of experimental medicine · 2015Review
- sRNA-Mediated Regulation of P-Fimbriae Phase Variation in Uropathogenic Escherichia coli.PLoS pathogens · 2015Article
- Non-coding RNA regulation in pathogenic bacteria located inside eukaryotic cells.Frontiers in cellular and infection microbiology · 2014Review
- Small RNA-mediated regulation of host-pathogen interactions.Virulence · 2013Review
- Identifying and characterizing Hfq-RNA interactions.Methods (San Diego, Calif.) · 2013Review
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Francisella tularensis is a highly virulent bacterium responsible for the zoonotic disease tularemia. It is a facultative intracellular pathogen that replicates in the cytoplasm of host cells, particularly in macrophages. Here we show that F. tularensis live vaccine strain (LVS) expresses a novel small RNA (sRNA), which modulates the virulence capacities of the bacterium. When this sRNA, designated FtrC (for Francisella tularensis RNA C), is expressed at high levels, F. tularensis replicates in macrophages less efficiently than the wild-type parent strain. Similarly, high expression of FtrC reduces the number of viable bacteria recovered from the spleen and liver of infected mice. Our data demonstrate that expression of gene FTL_1293 is regulated by FtrC. Furthermore, we show by in vitro gel shift assays that FtrC interacts specifically with FTL_1293 mRNA and that this happens independently of the RNA chaperone Hfq. Remarkably, FtrC interacts only with full-length FTL_1293 mRNA. These results, combined with a bioinformatic analysis, indicate that FtrC interacts with the central region of the mRNA and hence does not act by sterically hindering access of the ribosome to the mRNA. We further show that gene FTL_1293 is not required for F. tularensis virulence in vitro or in vivo, which indicates that another unidentified FtrC target modulates the virulence capacity of the bacterium.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.