ArticleMolecular microbiology2019
Analysis of a flagellar filament cap mutant reveals that HtrA serine protease degrades unfolded flagellin protein in the periplasm of Borrelia burgdorferi.
Article in Molecular microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Lyme-Borreliosis Disease: IgM Epitope Mapping and Evaluation of a Serological Assay Based on Immunodominant Bi-Specific Peptides.Biomedicines · 2025Article
- The Flagellin-Specific Chaperone FliS of Borrelia burgdorferi Controls the Cytoplasmic Pool of Flagellins at the Level of Translation Initiation, Secretion, and Proteolysis.Molecular microbiology · 2025Article
- Borrelia burgdorferi serine protease HtrA is a pleiotropic regulator of stress response, motility, flagellar hemostasis, and infectivity.Communications biology · 2025Article
- Broadly conserved FlgV controls flagellar assembly and Borrelia burgdorferi dissemination in mice.Nature communications · 2024Article
- Structural diversity and clustering of bacterial flagellar outer domains.Nature communications · 2024Article
- Broadly conserved FlgV controls flagellar assembly andbioRxiv : the preprint server for biology · 2024Article
- A chemosensory-like histidine kinase is dispensable for chemotaxis in vitro but regulates the virulence of Borrelia burgdorferi through modulating the stability of RpoS.PLoS pathogens · 2023Article
- Application of biophysical methods for improved protein production and characterization: A case study on an high-temperature requirement A-family bacterial protease.Protein science : a publication of the Protein Society · 2022Article
- A Regulatory SRNA Rli43 Is Involved in the Modulation of Biofilm Formation and Virulence inPathogens (Basel, Switzerland) · 2022Article
- BB0761, a MepM homolog, contributes to Borrelia burgdorferi cell division and mammalian infectivity.Molecular microbiology · 2022Article
- Controlled Proteolysis of an Essential Virulence Determinant Dictates Infectivity of Lyme Disease Pathogens.Infection and immunity · 2022Article
- Endogenous and Borrowed Proteolytic Activity in theMicrobiology and molecular biology reviews : MMBR · 2021Review
- Lyme Disease Pathogenesis.Current issues in molecular biology · 2021Review
- Structural Conservation and Adaptation of the Bacterial Flagella Motor.Biomolecules · 2020Review
- FlhF regulates the number and configuration of periplasmic flagella in Borrelia burgdorferi.Molecular microbiology · 2020Article
- The Lon-1 Protease Is Required by Borrelia burgdorferi To Infect the Mammalian Host.Infection and immunity · 2020Article
- Architecture and Assembly of Periplasmic Flagellum.Microbiology spectrum · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Unlike external flagellated bacteria, spirochetes have periplasmic flagella (PF). Very little is known about how PF are assembled within the periplasm of spirochaetal cells. Herein, we report that FliD (BB0149), a flagellar cap protein (also named hook-associated protein 2), controls flagellin stability and flagellar filament assembly in the Lyme disease spirochete Borrelia burgdorferi. Deletion of fliD leads to non-motile mutant cells that are unable to assemble flagellar filaments and pentagon-shaped caps (10 nm in diameter, 12 nm in length). Interestingly, FlaB, a major flagellin protein of B. burgdorferi, is degraded in the fliD mutant but not in other flagella-deficient mutants (i.e., in the hook, rod, or MS-ring). Biochemical and genetic studies reveal that HtrA, a serine protease of B. burgdorferi, controls FlaB turnover. Specifically, HtrA degrades unfolded but not polymerized FlaB, and deletion of htrA increases the level of FlaB in the fliD mutant. Collectively, we propose that the flagellar cap protein FliD promotes flagellin polymerization and filament growth in the periplasm. Deletion of fliD abolishes this process, which leads to leakage of unfolded FlaB proteins into the periplasm where they are degraded by HtrA, a protease that prevents accumulation of toxic products in the periplasm.
Indexed as
Identifiers
What OpenQuestion holds
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.