ArticlePloS one2013
Increasing RpoS expression causes cell death in Borrelia burgdorferi.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Innate immune responses tomBio · 2026Article
- DNA Binding by BosR Controls RpoS-Dependent and -Independent Gene Expression in Borrelia burgdorferi.Molecular microbiology · 2026Article
- 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
- Structure of phosphorylated-like RssB, the adaptor delivering σThe Journal of biological chemistry · 2023Article
- BosR and PlzA reciprocally regulate RpoS function to sustain Borrelia burgdorferi in ticks and mammals.The Journal of clinical investigation · 2023Article
- Coupled induction of prophage and virulence factors during tick transmission of the Lyme disease spirochete.Nature communications · 2023Article
- Genetic Manipulation ofCurrent issues in molecular biology · 2021Review
- Evidence that BosR (BB0647) Is a Positive Autoregulator in Borrelia burgdorferi.Infection and immunity · 2016Article
- Insight into the Dual Functions of Bacterial Enhancer-Binding Protein Rrp2 of Borrelia burgdorferi.Journal of bacteriology · 2016Article
- Use of an endogenous plasmid locus for stable in trans complementation in Borrelia burgdorferi.Applied and environmental microbiology · 2015Article
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
RpoS, one of the two alternative σ factors in Borrelia burgdorferi, is tightly controlled by multiple regulators and, in turn, determines expression of many critical virulence factors. Here we show that increasing RpoS expression causes cell death. The immediate effect of increasing RpoS expression was to promote bacterial division and as a consequence result in a rapid increase in cell number before causing bacterial death. No DNA fragmentation or degradation was observed during this induced cell death. Cryo-electron microscopy showed induced cells first formed blebs, which were eventually released from dying cells. Apparently blebbing initiated cell disintegration leading to cell death. These findings led us to hypothesize that increasing RpoS expression triggers intracellular programs and/or pathways that cause spirochete death. The potential biological significance of induced cell death may help B. burgdorferi regulate its population to maintain its life cycle in nature.
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.