ArticleInfection and immunity2011
Analysis of the Borrelia burgdorferi cyclic-di-GMP-binding protein PlzA reveals a role in motility and virulence.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 60 papers.
What it found
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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.
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.
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Who cites it
60 citing papers in PubMed, 85 citations in OpenAlex.
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- Analysis of the BadR regulon in Borrelia burgdorferi.BMC microbiology · 2025Article
- Insertion of a Divergent GAF-like Domain Defines a Novel Family of YcgR Homologues That Bind c-di-GMP inACS omega · 2025Article
- Article
- c-di-GMP regulates activity of the PlzA RNA chaperone from the Lyme disease spirochete.Molecular microbiology · 2023Article
- BosR and PlzA reciprocally regulate RpoS function to sustain Borrelia burgdorferi in ticks and mammals.The Journal of clinical investigation · 2023Article
- The Involvement of Thiamine Uptake in the Virulence ofPathogens (Basel, Switzerland) · 2022Article
- Potential Regulatory Role in Mammalian Host Adaptation for a Small Intergenic Region of Lp17 in the Lyme Disease Spirochete.Frontiers in cellular and infection microbiology · 2022Article
- Article
- PlzA is a bifunctional c-di-GMP biosensor that promotes tick and mammalian host-adaptation of Borrelia burgdorferi.PLoS pathogens · 2021Article
- High-resolution crystal structure of the Borreliella burgdorferi PlzA protein in complex with c-di-GMP: new insights into the interaction of c-di-GMP with the novel xPilZ domain.Pathogens and disease · 2021Article
- Interactions between Borrelia burgdorferi and its hosts across the enzootic cycle.Parasite immunology · 2021Review
- Motility, Adhesion and c-di-GMP Influence the Endophytic Colonization of Rice byMicroorganisms · 2021Article
- Interactions Between Ticks and Lyme Disease Spirochetes.Current issues in molecular biology · 2021Article
- Multiple CheY Proteins Control Surface-Associated Lifestyles ofFrontiers in microbiology · 2021Article
- Lyme Disease Pathogenesis.Current issues in molecular biology · 2021Review
- Gene Regulation and Transcriptomics.Current issues in molecular biology · 2021Article
- BB0326 is responsible for the formation of periplasmic flagellar collar and assembly of the stator complex in Borrelia burgdorferi.Molecular microbiology · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The cyclic-dimeric-GMP (c-di-GMP)-binding protein PilZ has been implicated in bacterial motility and pathogenesis. Although BB0733 (PlzA), the only PilZ domain-containing protein in Borrelia burgdorferi, was reported to bind c-di-GMP, neither its role in motility or virulence nor it's affinity for c-di-GMP has been reported. We determined that PlzA specifically binds c-di-GMP with high affinity (dissociation constant [K(d)], 1.25 μM), consistent with K(d) values reported for c-di-GMP-binding proteins from other bacteria. Inactivation of the monocistronically transcribed plzA resulted in an opaque/solid colony morphology, whereas the wild-type colonies were translucent. While the swimming pattern of mutant cells appeared normal, on swarm plates, mutant cells exhibited a significantly reduced swarm diameter, demonstrating a role of plzA in motility. Furthermore, the plzA mutant cells were significantly less infectious in experimental mice (as determined by 50% infectious dose [ID(50)]) relative to wild-type spirochetes. The mutant also had survival rates in fed ticks lower than those of the wild type. Consequently, plzA mutant cells failed to complete the mouse-tick-mouse infection cycle, indicating plzA is essential for the enzootic life cycle of B. burgdorferi. All of these defects were corrected when the mutant was complemented in cis. We propose that failure of plzA mutant cells to infect mice was due to altered motility; however, the possibility that an unidentified factor(s) contributed to interruption of the B. burgdorferi enzootic life cycle cannot yet be excluded.
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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.