ArticleNucleic acids research2024
Transposition with Tn3-family elements occurs through interaction with the host β-sliding clamp processivity factor.
Article in Nucleic acids research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Progresses of transposon research inSynthetic and systems biotechnology · 2026Review
- Ulva fasciata litter decomposition fuels microbial restructuring and antibiotic resistance proliferation in mariculture sediment.Antonie van Leeuwenhoek · 2026Article
- Phage Mu enlists the β-sliding clamp for late gene transcription.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Genetic and phenotypic characterization of the plasmid-encoded NDM-80 metallo-β-lactamase inFrontiers in microbiology · 2026Article
- Pathogen virulence genes: Advances, challenges and future directions in infectious disease research (Review).International journal of molecular medicine · 2025Review
- Transmission dynamics of ST346 carbapenem-resistantiScience · 2025Article
- Influence of Different Transposon Families on Genomic Stability of Shewanella oneidensis MR1.Microbial biotechnology · 2025Article
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11 authors.
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Abstract
Tn3 family transposons are a widespread group of replicative transposons, notorious for contributing to the dissemination of antibiotic resistance, particularly the global prevalence of carbapenem resistance. The transposase (TnpA) of these elements catalyzes DNA breakage and rejoining reactions required for transposition. However, the molecular mechanism for target site selection with these elements remains unclear. Here, we identify a QLxxLR motif in N-terminal of Tn3 TnpAs and demonstrate that this motif allows interaction between TnpA of Tn3 family transposon Tn1721 and the host β-sliding clamp (DnaN), the major processivity factor of the DNA replication machinery. The TnpA-DnaN interaction is essential for Tn1721 transposition. Our work unveils a mechanism whereby Tn3 family transposons can bias transposition into certain replisomes through an interaction with the host replication machinery. This study further expands the diversity of mobile elements that use interaction with the host replication machinery to bias integration.
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