ArticleMicrobiology (Reading, England)2015
The Fur homologue BosR requires Arg39 to activate rpoS transcription in Borrelia burgdorferi and thereby direct spirochaete infection in mice.
Article in Microbiology (Reading, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
- TheInfection and immunity · 2026Article
- The BosR Is Back!Molecular microbiology · 2026Article
- DNA Binding by BosR Controls RpoS-Dependent and -Independent Gene Expression in Borrelia burgdorferi.Molecular microbiology · 2026Article
- Virulence Regulation inMicroorganisms · 2025Review
- Article
- A Fur family protein BosR is a novel RNA-binding protein that controls rpoS RNA stability in the Lyme disease pathogen.Nucleic acids research · 2024Article
- Proteomic analysis reveals the adaptation of Vibrio splendidus to an iron deprivation condition.Applied microbiology and biotechnology · 2023Article
- Gene Regulation and Transcriptomics.Current issues in molecular biology · 2021Article
- Borrelia burgdorferi spatiotemporal regulation of transcriptional regulator bosR and decorin binding protein during murine infection.Scientific reports · 2020Article
- The CXXC Motifs Are Essential for the Function of BosR inFrontiers in cellular and infection microbiology · 2019Article
- Borrelia burgdorferi genes, bb0639-0642, encode a putative putrescine/spermidine transport system, PotABCD, that is spermidine specific and essential for cell survival.Molecular microbiology · 2018Article
- The Stringent Response-Regulated sRNA Transcriptome ofFrontiers in cellular and infection microbiology · 2018Article
- Weak Organic Acids DecreaseFrontiers in microbiology · 2017Article
- Gene bb0318 Is Critical for the Oxidative Stress Response and Infectivity of Borrelia burgdorferi.Infection and immunity · 2016Article
- Evidence that BosR (BB0647) Is a Positive Autoregulator in Borrelia burgdorferi.Infection and immunity · 2016Article
- Gene Regulation During the Enzootic Cycle of the Lyme Disease Spirochete.Forum on immunopathological diseases and therapeutics · 2016Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Borrelia burgdorferi is the causative agent of Lyme disease. In B. burgdorferi, RpoS controls the expression of virulence genes needed for mammalian infection. The Fur homologue BosR regulates the transcription of rpoS and therefore BosR determines, albeit indirectly, the infection status of the spirochaete. Transcription of rpoS in B. burgdorferi is complex: rpoS can be transcribed either from an RpoD-dependent promoter to yield a long transcript or from an RpoN-dependent promoter to yield a short transcript. This study shows that BosR repressed synthesis of the long transcript while at the same time activating synthesis of the short transcript. How BosR does this is unclear. To address this, spirochaetes were engineered to express either BosR or the naturally occurring variant BosRR39K. Mice became infected by the spirochaetes expressing BosR but not by the spirochaetes expressing BosRR39K. Furthermore, the spirochaetes expressing BosR activated rpoS transcription during growth in culture whereas the spirochaetes expressing BosRR39K did not. Thus, BosR's activation of rpoS transcription somehow involves Arg39. This arginine is highly conserved in other FUR proteins and therefore other FUR proteins may also require this arginine to function.
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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.