Evidence map›Paper›PMID 28542496›Full record

ArticlePloS one2017

Zinc blocks SOS-induced antibiotic resistance via inhibition of RecA in Escherichia coli.

Bryan E Bunnell, Jillian F Escobar, Kirsten L Bair, Mark D Sutton, John K Crane

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

37 citing papers in PubMed, 59 citations in OpenAlex.

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  11. mLife · 2024
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  13. The Multifaceted Actions of PVP-Curcumin for Treating Infections.International journal of molecular sciences · 2024
    Article
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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

5 authors at 1 institution in 1 country.

Bryan E BunnellDepartment of Medicine, Division of Infectious Diseases, University at Buffalo, Buffalo, NY, United States of America.
Jillian F EscobarDepartment of Medicine, Division of Infectious Diseases, University at Buffalo, Buffalo, NY, United States of America.
Kirsten L BairDepartment of Medicine, Division of Infectious Diseases, University at Buffalo, Buffalo, NY, United States of America.
Mark D SuttonDepartment of Biochemistry, University at Buffalo, Buffalo, NY, United States of America.
John K CraneDepartment of Medicine, Division of Infectious Diseases, University at Buffalo, Buffalo, NY, United States of America.ORCID http://orcid.org/0000-0002-1341-5665
University at Buffalo, State University of New York · US

Funding

University of Buffalo Clinical and Translational Science Institute - Supplement SchulyerUL1TR001412 · NCATS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI MURPHY, TIMOTHY F · 2015 to 2024
$33.8M
Effect of Zinc in Attaching and Effacing E. coli InfectionR01AI081528 · NIAID · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI BOEDEKER, EDGAR C., CRANE, JOHN K. · 2010 to 2012
$1.4M
Training the Next Generation of Physician ScientistsT35AI089693 · NIAID · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI Mark Daniel Hicar · 2011 to 2026
$689k
Enhancing Host Intestinal Defenses against Enteropathogenic and Shiga toxigenic ER21AI102212 · NIAID · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI CRANE, JOHN K. · 2012 to 2013
$415k
NCATS NIH HHS UL1 TR001412NIAID NIH HHS R01 AI081528NIAID NIH HHS R21 AI102212NIAID NIH HHS T35 AI089693
6 · The paper itself

Abstract

Zinc inhibits the virulence of diarrheagenic E. coli by inducing the envelope stress response and inhibiting the SOS response. The SOS response is triggered by damage to bacterial DNA. In Shiga-toxigenic E. coli, the SOS response strongly induces the production of Shiga toxins (Stx) and of the bacteriophages that encode the Stx genes. In E. coli, induction of the SOS response is accompanied by a higher mutation rate, called the mutator response, caused by a shift to error-prone DNA polymerases when DNA damage is too severe to be repaired by canonical DNA polymerases. Since zinc inhibited the other aspects of the SOS response, we hypothesized that zinc would also inhibit the mutator response, also known as hypermutation. We explored various different experimental paradigms to induce hypermutation triggered by the SOS response, and found that hypermutation was induced not just by classical inducers such as mitomycin C and the quinolone antibiotics, but also by antiviral drugs such as zidovudine and anti-cancer drugs such as 5-fluorouracil, 6-mercaptopurine, and azacytidine. Zinc salts inhibited the SOS response and the hypermutator phenomenon in E. coli as well as in Klebsiella pneumoniae, and was more effective in inhibiting the SOS response than other metals. We then attempted to determine the mechanism by which zinc, applied externally in the medium, inhibits hypermutation. Our results show that zinc interferes with the actions of RecA, and protects LexA from RecA-mediated cleavage, an early step in initiation of the SOS response. The SOS response may play a role in the development of antibiotic resistance and the effect of zinc suggests ways to prevent it.

Indexed as

Anti-Bacterial AgentsDrug Resistance, MicrobialEscherichia coliGene Expression Regulation, BacterialMutationRec A RecombinasesSOS Response, GeneticsVirulenceZincAnti-Bacterial AgentsRec A RecombinasesZinc

Identifiers

PMID28542496
PMCPMC5440055
OpenAlexW2617205858

What OpenQuestion holds

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LicenceCC BY
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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.