Articlenpj antimicrobials and resistance2026
Mechanistic insights into plasmid transfer inhibition in Enterobacterales by nucleoside analogues.
Article in npj antimicrobials and resistance, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Rhein reduces conjugation of IncFII-type plasmids inMicrobiology spectrum · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Antimicrobial resistance (AMR) poses a major global health threat, with carbapenem-resistant and extended-spectrum β-lactamase (ESBL)-producing Enterobacterales causing widespread infections and deaths. Much of this resistance spreads through conjugative plasmids, autonomously replicating mobile genetic elements that transfer between bacteria and carry multiple AMR genes. Targeting plasmid conjugation could therefore help curb the spread of AMR. In this study, we tested whether clinically approved nucleoside analogues (NAs) inhibited the transfer of the GFP-tagged ESBL-encoding IncK plasmid pCTgfp in Escherichia coli and the carbapenemase-encoding IncF plasmid pKpQILgfp in Klebsiella pneumoniae using flow cytometry. Alongside the known inhibitor azidothymidine (AZT), didanosine, stavudine, and trifluridine reduced plasmid conjugation in both species without affecting growth. Conversely, famciclovir and zalcitabine promoted pCTgfp conjugation in E. coli, while aciclovir and valaciclovir enhanced pKpQILgfp conjugation in K. pneumoniae. Mechanistic studies showed that plasmid conjugation-promoting NAs altered intracellular ATP levels. RNA sequencing revealed that AZT downregulated the expression of genes linked to motility in E. coli. Genetic inactivation of motility in E. coli mirrored the decrease in pCTgfp conjugation, like AZT. In K. pneumoniae, AZT upregulated genes linked to DNA damage and the SOS response, but downregulated methionine biosynthesis and metabolism genes. The exogenous addition of zinc acetate to inhibit RecA or the end product of methionine metabolism, S-adenosyl-methionine, restored pKpQILgfp conjugation in K. pneumoniae. Overall, our results indicated that existing NAs, including AZT, represent structural scaffolds for the development of potent conjugation inhibitors and highlight motility, DNA repair, and methionine metabolism as potential key factors in plasmid conjugation.
Identifiers
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Registered trials
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.