ArticleRNA (New York, N.Y.)2014
Aminoglycoside resistance 16S rRNA methyltransferases block endogenous methylation, affect translation efficiency and fitness of the host.
Article in RNA (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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31 citing papers in PubMed, 50 citations in OpenAlex.
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- Functional shotgun metagenomic insights into gut microbial pathway and enzyme disruptions linking metabolism, affect, cognition, and suicidal ideation in major depressive disorder.Acta neuropsychiatrica · 2026Article
- Biological cost of aminoglycoside resistance Arm/Kam 16S rRNA methyltransferases from natural antibiotic producers and clinical pathogens.Antimicrobial agents and chemotherapy · 2025Article
- Emergence of NDM-1- and OXA-23-Co-ProducingMicroorganisms · 2025Article
- The newly identifiedAntimicrobial agents and chemotherapy · 2025Article
- Past, Present, and Future of RNA Modifications in Infectious Disease Research.ACS infectious diseases · 2024Article
- Polymorphism of virulence genes and biofilm associated with in vitro induced resistance to clarithromycin in Helicobacter pylori.Gut pathogens · 2023Article
- Functional analysis of bacterial genes accidentally packaged in rhizospheric phageome of the wild plant speciesSaudi journal of biological sciences · 2023Article
- 30S subunit recognition and G1405 modification by the aminoglycoside-resistance 16S ribosomal RNA methyltransferase RmtC.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- A panel of diverseMicrobial genomics · 2023Article
- 30S subunit recognition and G1405 modification by the aminoglycoside-resistance 16S ribosomal RNA methyltransferase RmtC.bioRxiv : the preprint server for biology · 2023Article
- Ribosome-targeting antibiotics and resistanceRSC medicinal chemistry · 2023Review
- Virotyping and genetic antimicrobial susceptibility testing of porcine ETEC/STEC strains and associated plasmid types.Frontiers in microbiology · 2023Article
- Interactions between host epithelial cells andEmerging microbes & infections · 2022Article
- Public health implications of plasmid-mediated quinolone and aminoglycoside resistance genes inEpidemiology and infection · 2022Article
- Review
- Molecular survey of aminoglycoside-resistantNew microbes and new infections · 2021Article
- Identification and Validation of Reference Genes inFrontiers in microbiology · 2021Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In Gram-negative bacteria, acquired 16S rRNA methyltransferases ArmA and NpmA confer high-level resistance to all clinically useful aminoglycosides by modifying, respectively, G1405 and A1408 in the A-site. These enzymes must coexist with several endogenous methyltransferases that are essential for fine-tuning of the decoding center, such as RsmH and RsmI in Escherichia coli, which methylate C1402 and RsmF C1407. The resistance methyltransferases have a contrasting distribution--ArmA has spread worldwide, whereas a single clinical isolate producing NpmA has been reported. The rate of dissemination of resistance depends on the fitness cost associated with its expression. We have compared ArmA and NpmA in isogenic Escherichia coli harboring the corresponding structural genes and their inactive point mutants cloned under the control of their native constitutive promoter in the stable plasmid pGB2. Growth rate determination and competition experiments showed that ArmA had a fitness cost due to methylation of G1405, whereas NpmA conferred only a slight disadvantage to the host due to production of the enzyme. MALDI MS indicated that ArmA impeded one of the methylations at C1402 by RsmI, and not at C1407 as previously proposed, whereas NpmA blocked the activity of RsmF at C1407. A dual luciferase assay showed that methylation at G1405 and A1408 and lack of methylation at C1407 affect translation accuracy. These results indicate that resistance methyltransferases impair endogenous methylation with different consequences on cell fitness.
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