ArticleCommunications biology2025
Comprehensive analysis of Enterobacteriaceae IncX plasmids reveals robust conjugation regulators PrfaH, H-NS, and conjugation-fitness tradeoff.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Effects of florfenicol on linezolid resistance in Enterococcus faecium from waterfowl farms.Poultry science · 2026Article
- Selective targeting of a histone-like silencer Sfx to the R6K conjugal transfer operon.Nucleic acids research · 2026Article
- Characteristics ofOne health (Amsterdam, Netherlands) · 2026Article
- Plasmid-resolved genomics and machine learning-assisted profiling revealFrontiers in microbiology · 2026Article
- Cross-species transmission ofFrontiers in cellular and infection microbiology · 2026Review
- Detection and Genomic Characteristics of NDM-19- and QnrS11-Producing O101:H5Microorganisms · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
Conjugative IncX plasmids are vital for spreading clinically significant antibiotic resistance genes. We identified key factors governing the conjugative process of IncX plasmids, the plasmid encoded activator PrfaH and inhibitor H-NS. Deletion of prfaH completely abolishes conjugative transfer, and the PrfaH binding site is an ops-like sequence located downstream of the prfaH promoter. We solved the crystal structure of PrfaH and identified the residues that likely mediate interactions with its target. The IncX3 plasmid-encoded H-NS inhibits conjugation by directly repressing PrfaH expression, while simultaneously enhancing host fitness. This tradeoff between plasmid conjugation and fitness is indispensable for plasmid persistence in nutrient-deprived environments. The presence of PrfaH paralogs in various antibiotic resistance plasmids suggests its fundamental role in regulating plasmid transfer. Our study not only elucidates the regulatory mechanisms behind the horizontal transfer of IncX plasmids but also highlights PrfaH as a potential target for strategies aimed at combating antimicrobial resistance.
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