Evidence map›Paper›PMID 35524246›Full record

ArticleJournal of biomedical science2022

Unravelling the physiological roles of mazEF toxin-antitoxin system on clinical MRSA strain by CRISPR RNA-guided cytidine deaminase.

Sonia Jain, Arghya Bhowmick, Bohyun Jeong, Taeok Bae, Abhrajyoti Ghosh

Open access · diamondAbstract read
In one paragraph

Article in Journal of biomedical science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. CRISPR-driven strategies to disrupt methicillin-resistantFrontiers in cellular and infection microbiology · 2026
    Review
  4. Review
  5. The Secondary Resistome of Methicillin-ResistantAntibiotics (Basel, Switzerland) · 2025
    Article
  6. Article
  7. Article
  8. The Benefits of Toxicity:Microorganisms · 2023
    Article
  9. 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

5 authors at 4 institutions in 3 countries.

Sonia JainInfectious Disease and Immunology Division, CSIR-Indian Institute of Chemical Biology, Kolkata, 700032, India. swtsoniajain@gmail.com.
Arghya BhowmickDepartment of Biochemistry, Bose Institute, EN Block, Sector-V, Kolkata, 700091, India.
Bohyun JeongDepartment of Microbiology, Kosin University College of Medicine, Busan, 49267, South Korea.
Taeok BaeDepartment of Microbiology and Immunology, Indiana University, School of Medicine-Northwest, Gary, IN, 46408-1197, USA.
Abhrajyoti GhoshDepartment of Biochemistry, Bose Institute, EN Block, Sector-V, Kolkata, 700091, India. aghosh78@gmail.com.
Bose Institute · INIndiana University Northwest · USIndian Institute of Chemical Biology · INKosin University · KR

Funding

The mechanism of the beta-lactam resistance in Staphylococcus aureusR01AI143792 · NIAID · INDIANA UNIVERSITY INDIANAPOLIS · PI BAE, TAEOK · 2020 to 2023
$1.6M
Department of Science and Technology, India SR/WOS-A/LS-1021/2015NIAID NIH HHS R01 AI143792Partially funded by Science and Engineering Research Board (SERB), Govt. of India CRG/2018/001732
6 · The paper itself

Abstract

backgroundCuriosity on toxin-antitoxin modules has increased intensely over recent years as it is ubiquitously present in many bacterial genomes, including pathogens like Methicillin-resistant Staphylococcus aureus (MRSA). Several cellular functions of TA systems have been proposed however, their exact role in cellular physiology remains unresolved.

methodsThis study aims to find out the impact of the mazEF toxin-antitoxin module on biofilm formation, pathogenesis, and antibiotic resistance in an isolated clinical ST239 MRSA strain, by constructing mazE and mazF mutants using CRISPR-cas9 base-editing plasmid (pnCasSA-BEC). Transcriptome analysis (RNA-seq) was performed for the mazE antitoxin mutant in order to identify the differentially regulated genes. The biofilm formation was also assessed for the mutant strains. Antibiogram profiling was carried out for both the generated mutants followed by murine experiment to determine the pathogenicity of the constructed strains.

resultsFor the first time our work showed, that MazF promotes cidA mediated cell death and lysis for biofilm formation without playing any significant role in host virulence as suggested by the murine experiment. Interestingly, the susceptibility to oxacillin, daptomycin and vancomycin was reduced significantly by the activated MazF toxin in the mazE mutant strain.

conclusionsOur study reveals that activated MazF toxin leads to resistance to antibiotics like oxacillin, daptomycin and vancomycin. Therefore, in the future, any potential antibacterial drug can be designed to target MazF toxin against the problematic multi-drug resistant bug.

Indexed as

DaptomycinMethicillin-Resistant Staphylococcus aureusToxin-Antitoxin SystemsAnimalsAnti-Bacterial AgentsBacterial ProteinsCytidine DeaminaseMiceOxacillinRNAVancomycinAnti-Bacterial AgentsBacterial ProteinsCytidine DeaminaseDaptomycinOxacillinRNAVancomycinAntibiotic resistanceBiofilmCRISPR–Cas9MRSAToxin–antitoxinVirulence

Identifiers

PMID35524246
PMCPMC9077811
OpenAlexW4229072936

What OpenQuestion holds

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LicenceCC BY
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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.