Evidence map›Paper›PMID 29235503›Full record

ArticleScientific reports2017

Inactivation of the dnaK gene in Clostridium difficile 630 Δerm yields a temperature-sensitive phenotype and increases biofilm-forming ability.

Shailesh Jain, Deborah Smyth, Barry M G O'Hagan, John T Heap, Geoff McMullan, Nigel P Minton, Nigel G Ternan

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.5field-weighted citation impact, top 19% of its field
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

31 citing papers in PubMed, 46 citations in OpenAlex.

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  8. Sortase-encoding genes,Frontiers in microbiology · 2024
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  12. Biofilm Formation ofMicroorganisms · 2023
    Review
  13. Non-Toxin-BasedPathogens (Basel, Switzerland) · 2023
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  15. Efficacy of Dry Heat Treatment againstPathogens (Basel, Switzerland) · 2022
    Article
  16. Article
  17. Article
  18. Wolf in Sheep's Clothing:Microorganisms · 2021
    Review
  19. Review
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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

7 authors at 4 institutions in 1 country.

Shailesh JainNutrition Innovation Centre for Food and HEalth (NICHE), School of Biomedical Sciences,University of Ulster, Coleraine, Co. Londonderry, N. Ireland, BT52 1SA, UK.
Deborah SmythNutrition Innovation Centre for Food and HEalth (NICHE), School of Biomedical Sciences,University of Ulster, Coleraine, Co. Londonderry, N. Ireland, BT52 1SA, UK.
Barry M G O'HaganNutrition Innovation Centre for Food and HEalth (NICHE), School of Biomedical Sciences,University of Ulster, Coleraine, Co. Londonderry, N. Ireland, BT52 1SA, UK.
John T HeapCentre for Synthetic Biology and Innovation, Department of Life Sciences, Imperial College London, South Kensington Campus, London, SW7 2AZ, UK.
Geoff McMullanInstitute for Global Food Security, School of Biological Sciences, Queen's University Belfast, N. Ireland, United Kingdom, BT9 7BL, UK.
Nigel P MintonClostridia Research Group, BBSRC/EPSRC Synthetic Biology Research Centre (SBRC), University of Nottingham, University Park, Nottingham, NG7 2RD, UK.
Nigel G TernanNutrition Innovation Centre for Food and HEalth (NICHE), School of Biomedical Sciences,University of Ulster, Coleraine, Co. Londonderry, N. Ireland, BT52 1SA, UK. ng.ternan@ulster.ac.uk.ORCID 0000-0002-1788-7571
University of Ulster · GBEngineering and Physical Sciences Research Council · GBImperial College London · GBQueen's University Belfast · GB

Funding

Medical Research Council G0601176
6 · The paper itself

Abstract

Clostridium difficile infection is a growing problem in healthcare settings worldwide and results in a considerable socioeconomic impact. New hypervirulent strains and acquisition of antibiotic resistance exacerbates pathogenesis; however, the survival strategy of C. difficile in the challenging gut environment still remains incompletely understood. We previously reported that clinically relevant heat-stress (37-41 °C) resulted in a classical heat-stress response with up-regulation of cellular chaperones. We used ClosTron to construct an insertional mutation in the dnaK gene of C. difficile 630 Δerm. The dnaK mutant exhibited temperature sensitivity, grew more slowly than C. difficile 630 Δerm and was less thermotolerant. Furthermore, the mutant was non-motile, had 4-fold lower expression of the fliC gene and lacked flagella on the cell surface. Mutant cells were some 50% longer than parental strain cells, and at optimal growth temperatures, they exhibited a 4-fold increase in the expression of class I chaperone genes including GroEL and GroES. Increased chaperone expression, in addition to the non-flagellated phenotype of the mutant, may account for the increased biofilm formation observed. Overall, the phenotype resulting from dnaK disruption is more akin to that observed in Escherichia coli dnaK mutants, rather than those in the Gram-positive model organism Bacillus subtilis.

Indexed as

Molecular ChaperonesBacterial ProteinsBiofilmsClostridioides difficileEscherichia coliGene Expression RegulationGene Knockout TechniquesMovementMutationPhenotypeTemperatureBacterial ProteinsMolecular Chaperones

Identifiers

PMID29235503
PMCPMC5727486
OpenAlexW2771460853

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.