ArticleMolecular microbiology2011
Carbon storage regulator A (CsrA(Bb)) is a repressor of Borrelia burgdorferi flagellin protein FlaB.
Article in Molecular microbiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 62 citations in OpenAlex.
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- Borrelia burgdorferi serine protease HtrA is a pleiotropic regulator of stress response, motility, flagellar hemostasis, and infectivity.Communications biology · 2025Article
- FlbB forms a distinctive ring essential for periplasmic flagellar assembly and motility in Borrelia burgdorferi.PLoS pathogens · 2025Article
- Chemotaxis Coupling Protein CheWInfection and immunity · 2023Article
- Identification and Characterization of the Alternative σJournal of bacteriology · 2022Article
- Transcriptional and functional characterizations of multiple flagellin genes in spirochetes.Molecular microbiology · 2022Article
- Review
- Gene Regulation and Transcriptomics.Current issues in molecular biology · 2021Article
- Article
- Contact with the CsrA Core Is Required for Allosteric Inhibition by FliW in Bacillus subtilis.Journal of bacteriology · 2020Article
- The BB0345 Hypothetical Protein of Borrelia burgdorferi Is Essential for Mammalian Infection.Infection and immunity · 2020Article
- FlhF regulates the number and configuration of periplasmic flagella in Borrelia burgdorferi.Molecular microbiology · 2020Article
- BB0326 is responsible for the formation of periplasmic flagellar collar and assembly of the stator complex in Borrelia burgdorferi.Molecular microbiology · 2020Article
- The Lyme disease spirochete's BpuR DNA/RNA-binding protein is differentially expressed during the mammal-tick infectious cycle, which affects translation of the SodA superoxide dismutase.Molecular microbiology · 2019Article
- Analysis of a flagellar filament cap mutant reveals that HtrA serine protease degrades unfolded flagellin protein in the periplasm of Borrelia burgdorferi.Molecular microbiology · 2019Article
- Article
- DksA Controls the Response of the Lyme Disease SpirocheteJournal of bacteriology · 2019Article
- Short-Chain Fatty Acids Alter Metabolic and Virulence Attributes of Borrelia burgdorferi.Infection and immunity · 2018Article
- Transcriptomic insights on the virulence-controlling CsrA, BadR, RpoN, and RpoS regulatory networks in the Lyme disease spirochete.PloS one · 2018Article
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6 authors at 1 institution in 1 country.
Funding
Abstract
The Lyme disease spirochete Borrelia burgdorferi lacks the transcriptional cascade control of flagellar protein synthesis common to other bacteria. Instead, it relies on a post-transcriptional mechanism to control its flagellar synthesis. The underlying mechanism of this control remains elusive. A recent study reported that the increased level of BB0184 (CsrA(Bb); a homologue of carbon storage regulator A) substantially inhibited the accumulation of FlaB, the major flagellin protein of B. burgdorferi. In this report, we deciphered the regulatory role of CsrA(Bb) on FlaB synthesis and the mechanism involved by analysing two mutants, csrA(Bb)(-) (a deletion mutant of csrA(Bb)) and csrA(Bb)(+) (a mutant conditionally overexpressing csrA(Bb)). We found that FlaB accumulation was significantly inhibited in csrA(Bb)(+) but was substantially increased in csrA(Bb)(-) . In contrast, the levels of other flagellar proteins remained unchanged. Cryo-electron tomography and immuno-fluorescence microscopic analyses revealed that the altered synthesis of CsrA(Bb) in these two mutants specifically affected flagellar filament length. The leader sequence of flaB transcript contains two conserved CsrA-binding sites, with one of these sites overlapping the Shine-Dalgarno sequence. We found that CsrA(Bb) bound to the flaB transcripts via these two binding sites, and this binding inhibited the synthesis of FlaB at the translational level. Taken together, our results indicate that CsrA(Bb) specifically regulates the periplasmic flagellar synthesis by inhibiting translation initiation of the flaB transcript.
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