Evidence map›Paper›PMID 27386955›Full record

ArticleScientific reports2016

CpsR, a GntR family regulator, transcriptionally regulates capsular polysaccharide biosynthesis and governs bacterial virulence in Streptococcus pneumoniae.

Kaifeng Wu, Hongmei Xu, Yuqiang Zheng, Libin Wang, Xuemei Zhang, Yibing Yin

Abstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed.

  1. Trial
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  12. MgaVirulence · 2021
    Article
  13. Biology · 2021
    Article
  14. Review
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  20. Identification of a GntR family regulator BusRExtremophiles : life under extreme conditions · 2019
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Kaifeng WuKey Laboratory of Diagnostic Medicine designated by the Ministry of Education, Chongqing Medical University, Chongqing 400016, People's republic of China.
Hongmei XuKey Laboratory of Diagnostic Medicine designated by the Ministry of Education, Chongqing Medical University, Chongqing 400016, People's republic of China.
Yuqiang ZhengKey Laboratory of Diagnostic Medicine designated by the Ministry of Education, Chongqing Medical University, Chongqing 400016, People's republic of China.
Libin WangKey Laboratory of Diagnostic Medicine designated by the Ministry of Education, Chongqing Medical University, Chongqing 400016, People's republic of China.
Xuemei ZhangKey Laboratory of Diagnostic Medicine designated by the Ministry of Education, Chongqing Medical University, Chongqing 400016, People's republic of China.
Yibing YinKey Laboratory of Diagnostic Medicine designated by the Ministry of Education, Chongqing Medical University, Chongqing 400016, People's republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcriptional regulation of capsule expression is critical for pneumococcal transition from carriage to infection, yet the underlying mechanism remains incompletely understood. Here, we describe the regulation of capsular polysaccharide, one of the most important pneumococcal virulence factor by a GntR family regulator, CpsR. Electrophoretic mobility-shift assays have shown the direct interaction between CpsR and the cps promoter (cpsp), and their interaction could be competitively interfered by glucose. DNase I footprinting assays localized the binding site to a region -146 to -114 base pairs relative to the transcriptional start site of the cps locus in S. pneumoniae D39. We found that CpsR negatively controlled the transcription of the cps locus and hence CPS production, which was confirmed by fine-tuning expression of CpsR in a ΔcpsR complemented strain. Increased expression of CpsR in complemented strain led to a decreased resistance to the whole-blood-mediated killing, suggesting a protective role for CpsR-cpsp interaction in the establishment of invasive infection. Finally, animal experiments showed that CpsR-cpsp interaction was necessary for both pneumococcal colonization and invasive infection. Taken together, our results provide a thorough insight into the regulation of capsule production mediated by CpsR and its important roles in pneumococcal pathogenesis.

Indexed as

Gene Expression Regulation, BacterialAnimalsBacterial ProteinsBinding SitesBlood Bactericidal ActivityDNA, BacterialDNA FootprintingElectrophoretic Mobility Shift AssayGene DeletionGenetic Complementation TestMice, Inbred BALB CPneumococcal InfectionsPolysaccharides, BacterialPromoter Regions, GeneticProtein BindingStreptococcus pneumoniaeBacterial ProteinsDNA, BacterialPolysaccharides, BacterialTranscription Factors

Identifiers

PMID27386955
PMCPMC4937376

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Registered trials

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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.