Evidence map›Paper›PMID 27025643›Full record

ArticleAntibiotics (Basel, Switzerland)2015

Genetic Screen Reveals the Role of Purine Metabolism in Staphylococcus aureus Persistence to Rifampicin.

Rebecca Yee, Peng Cui, Wanliang Shi, Jie Feng, Ying Zhang

Open access · goldAbstract read
In one paragraph

Article in Antibiotics (Basel, Switzerland), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

53 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
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  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Bacterial persisters: molecular mechanisms and therapeutic development.Signal transduction and targeted therapy · 2024
    Review
  17. Article
  18. Article
  19. Article
  20. mBio · 2024
    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 1 institution in 1 country.

Rebecca YeeDepartment of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA. ryee2@jhu.edu.
Peng CuiDepartment of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA. keanuc@163.com.
Wanliang ShiDepartment of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA. wshi3@jhu.edu.
Jie FengDepartment of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA. jfeng16@jhu.edu.
Ying ZhangDepartment of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA. yzhang@jhsph.edu.
Johns Hopkins University · US

Funding

Training: Molecular & Cellular Bases of Infectious DiseasesT32AI007417 · NIAID · JOHNS HOPKINS UNIVERSITY · PI Arturo Casadevall · 1994 to 2026
$11.9M
Pyrazinamide and Trans-Translation in Mycobacterium tuberculosisR01AI099512 · NIAID · JOHNS HOPKINS UNIVERSITY · PI ZHANG, YING · 2012 to 2015
$1.7M
Toxin-antitoxins & RpsA in TB drug resistance & persistence with HIVR21AI108535 · NIAID · JOHNS HOPKINS UNIVERSITY · PI ZHANG, YING · 2014 to 2015
$443k
NIAID NIH HHS R01 AI099512NIAID NIH HHS R21 AI108535NIAID NIH HHS T32 AI007417
6 · The paper itself

Abstract

Chronic infections with Staphylococcus aureus such as septicemia, osteomyelitis, endocarditis, and biofilm infections are difficult to treat because of persisters. Despite many efforts in understanding bacterial persistence, the mechanisms of persister formation in S. aureus remain elusive. Here, we performed a genome-wide screen of a transposon mutant library to study the molecular mechanisms involved in persistence of community-acquired S. aureus. Screening of the library for mutants defective in persistence or tolerance to rifampicin revealed many genes involved in metabolic pathways that are important for antibiotic persistence. In particular, the identified mutants belonged to metabolic pathways involved in carbohydrate, amino acid, lipid, vitamin and purine biosynthesis. Five mutants played a role in purine biosynthesis and two mutants, purB, an adenylosuccinate lyase, and purM, a phosphoribosylaminoimidazole synthetase, were selected for further confirmation. Mutants purB and purM showed defective persistence compared to the parental strain USA300 in multiple stress conditions including various antibiotics, low pH, and heat stress. The defect in persistence was restored by complementation with the wildtype purB and purM gene in the respective mutants. These findings provide new insights into the mechanisms of persistence in S. aureus and provide novel therapeutic targets for developing more effective treatment for persistent infections due to S. aureus.

Indexed as

persisterspurinesrifampicinStaphylococcus aureus

Identifiers

PMID27025643
PMCPMC4790316
OpenAlexW2183179359

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.