ArticlePLoS genetics2023
Genetic basis of I-complex plasmid stability and conjugation.
Article in PLoS genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Pathogenome and Plasmid-Borne Antimicrobial Resistance Phenotypes in a Multidrug-Resistant O111:H8 Shiga Toxin-ProducingbioRxiv : the preprint server for biology · 2026Article
- Genetic traits of IncK2 plasmids and theMicrobial genomics · 2026Article
- Cross-species transmission ofFrontiers in cellular and infection microbiology · 2026Review
- Convergence of plasmid-driven virulence and antibiotic resistance in Escherichia coli.Nature communications · 2025Article
- Plasmid-mediated carbapenem resistance: global dissemination patterns and replicon-gene associations.International microbiology : the official journal of the Spanish Society for Microbiology · 2025Article
- Genetic determinants of pOXA-48 plasmid maintenance and propagation in Escherichia coli.Nature communications · 2025Article
- Exploration of the advantages of targeted isolation of deep-sea microorganisms and genetically engineered strains.World journal of microbiology & biotechnology · 2024Review
- Modified TnApplied and environmental microbiology · 2024Article
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Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Plasmids are major drivers of increasing antibiotic resistance, necessitating an urgent need to understand their biology. Here we describe a detailed dissection of the molecular components controlling the genetics of I-complex plasmids, a group of antibiotic resistance plasmids found frequently in pathogenic Escherichia coli and other Enterobacteriaceae that cause significant human disease. We show these plasmids cluster into four distinct subgroups, with the prototype IncI1 plasmid R64 subgroup displaying low nucleotide sequence conservation to other I-complex plasmids. Using pMS7163B, an I-complex plasmid distantly related to R64, we performed a high-resolution transposon-based genetic screen and defined genes involved in replication, stability, and conjugative transfer. We identified the replicon and a partitioning system as essential for replication/stability. Genes required for conjugation included the type IV secretion system, relaxosome, and several uncharacterised genes located in the pMS7163B leading transfer region that exhibited an upstream strand-specific transposon insertion bias. The overexpression of these genes severely impacted host cell growth or reduced fitness during mixed competitive growth, demonstrating that their expression must be controlled to avoid deleterious impacts. These genes were present in >80% of all I-complex plasmids and broadly conserved across multiple plasmid incompatibility groups, implicating an important role in plasmid dissemination.
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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.