Evidence map›Paper›PMID 29884863›Full record

ArticleThe Journal of antibiotics2018

Instability of the 16S rRNA methyltransferase-encoding npmA gene: why have bacterial cells possessing npmA not spread despite their high and broad resistance to aminoglycosides?

Yoshimasa Ishizaki, Yuko Shibuya, Chigusa Hayashi, Kunio Inoue, Teruo Kirikae, Tatsuya Tada, Tohru Miyoshi-Akiyama, Masayuki Igarashi

Abstract read
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In one paragraph

Article in The Journal of antibiotics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.2field-weighted citation impact, top 61% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Ribosome-targeting antibiotics and resistanceRSC medicinal chemistry · 2023
    Review
  5. Review
  6. Review
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

8 authors at 3 institutions in 1 country.

Yoshimasa IshizakiLaboratory of Microbiology, Institute of Microbial Chemistry, Tokyo, Japan. ishizakiy@bikaken.or.jp.
Yuko ShibuyaLaboratory of Microbiology, Institute of Microbial Chemistry, Tokyo, Japan.
Chigusa HayashiLaboratory of Microbiology, Institute of Microbial Chemistry, Tokyo, Japan.
Kunio InoueLaboratory of Microbiology, Institute of Microbial Chemistry, Tokyo, Japan.
Teruo KirikaeDepartment of Microbiology, Juntendo University School of Medicine, Tokyo, Japan.
Tatsuya TadaDepartment of Microbiology, Juntendo University School of Medicine, Tokyo, Japan.
Tohru Miyoshi-AkiyamaPathogenic Microbe Laboratory, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Masayuki IgarashiLaboratory of Microbiology, Institute of Microbial Chemistry, Tokyo, Japan.
Microbial Chemistry Research Foundation · JPJuntendo University · JPNational Center for Global Health and Medicine · JP

Funding

Japan Agency for Medical Research and Development (AMED) 16fk0108120j0001
6 · The paper itself

Abstract

The NpmA bacterial 16S rRNA methyltransferase, which is identified from Escherichia coli strains, confers high resistance to many types of aminoglycoside upon its host cells. But despite its resistance-conferring ability, only two cases of its isolation from E. coli (14 years apart) have been reported to date. Here, we investigated the effect of the npmA gene on aminoglycoside resistance in Pseudomonas aeruginosa and Klebsiella pneumoniae and its stability in E. coli cells by comparing it with armA, another 16S rRNA methyltransferase gene currently spreading globally. As a result, we found that npmA conferred resistance to all types of aminoglycoside antibiotics we tested (except streptomycin) in both P. aeruginosa and K. pneumoniae, as well in E. coli. In addition, co-expression of armA and npmA resulted in an additive effect for the resistance. However, in return for the resistance, we also observed that the growth rates and the cell survivability of the strains transformed with the npmA-harboring plasmids were inferior than those of the control strains and that these plasmids were easily disrupted by IS10, IS1, and IS5 insertion sequences. We discuss these data in the context of the threat posed by pathogenic strains possessing npmA.

Indexed as

AminoglycosidesAnti-Bacterial AgentsDrug Resistance, BacterialEscherichia coliEscherichia coli ProteinsKlebsiella pneumoniaeMethyltransferasesMicrobial Sensitivity TestsPlasmidsPseudomonas aeruginosaAminoglycosidesAnti-Bacterial AgentsArmA protein, E coliEscherichia coli ProteinsMethyltransferasesNpmA protein, E coli

Identifiers

PMID29884863
OpenAlexW2806768078

What OpenQuestion holds

Textmetadata
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.