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Peer-reviewedCC BY 4.0Nature Communications

Mobile genetic elements drive a plasmid fusion and deletion lifecycle shaping evolution and antimicrobial resistance

  • Thomas Ipoutcha1,2
  • Yiqing Wang3
  • Eduardo P C Rocha3
  • José R Penadés4,5,6
6 affiliations
  1. 1Department of Infectious Disease, Imperial College London, London, UK. [email protected].
  2. 2Centre for Bacterial Resistance Biology, Imperial College London, London, UK. [email protected].
  3. 3Institut Pasteur, Université de Paris Cité, CNRS UMR3525, Microbial Evolutionary Genomics, Paris, France.
  4. 4Department of Infectious Disease, Imperial College London, London, UK. [email protected].
  5. 5Centre for Bacterial Resistance Biology, Imperial College London, London, UK. [email protected].
  6. 6Veterinary School, Universidad CEU Cardenal Herrera, Alfara del Patriarca, Spain. [email protected].
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Abstract

Plasmids are key drivers of bacterial adaptation, yet the mechanisms that generate their diversity remain poorly understood. Here, we show that mobile genetic elements (MGEs) orchestrate a fusion-deletion life cycle that repeatedly remodels plasmids in Staphylococcus aureus . Large-scale genomic analyses reveal that multireplicon plasmids are widespread and strongly enriched in transposases. Using experimental assays, we demonstrate that rare MGE-mediated fusion events, via homologous recombination or transposition, combine distinct plasmids into single multireplicon elements, expanding gene content and transfer potential. Antibiotic pressure selectively enriches these fused plasmids, rescuing bacterial populations under stress, whereas opposing selective forces, including phage predation, favour deletion derivatives that preserve essential functions and phage transmissibility. This cyclical process generates dynamic plasmid repertoires with conserved backbones and diverse accessory modules. We propose that MGE-driven fusion-deletion cycles represent a general principle of plasmid evolution, explaining the rapid emergence and persistence of multidrug-resistant plasmids across bacterial pathogens.

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Cite

BibTeXRIS
BibTeX
@article{ipoutcha2026mobile,
  title = {{Mobile genetic elements drive a plasmid fusion and deletion lifecycle shaping evolution and antimicrobial resistance}},
  author = {Thomas Ipoutcha and Yiqing Wang and Eduardo P C Rocha and José R Penadés},
  journal = {Nature Communications},
  year = {2026},
  month = sep,
  doi = {10.1038/s41467-026-77678-8},
  url = {https://hal.science/hal-05764855v1},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Mobile genetic elements drive a plasmid fusion and deletion lifecycle shaping evolution and antimicrobial resistance
AU  - Thomas Ipoutcha
AU  - Yiqing Wang
AU  - Eduardo P C Rocha
AU  - José R Penadés
PY  - 2026
DA  - 2026/09/15
JO  - Nature Communications
DO  - 10.1038/s41467-026-77678-8
UR  - https://hal.science/hal-05764855v1
AB  - Plasmids are key drivers of bacterial adaptation, yet the mechanisms that generate their diversity remain poorly understood. Here, we show that mobile genetic elements (MGEs) orchestrate a fusion-deletion life cycle that repeatedly remodels plasmids in Staphylococcus aureus . Large-scale genomic analyses reveal that multireplicon plasmids are widespread and strongly enriched in transposases. Using experimental assays, we demonstrate that rare MGE-mediated fusion events, via homologous recombination or transposition, combine distinct plasmids into single multireplicon elements, expanding gene content and transfer potential. Antibiotic pressure selectively enriches these fused plasmids, rescuing bacterial populations under stress, whereas opposing selective forces, including phage predation, favour deletion derivatives that preserve essential functions and phage transmissibility. This cyclical process generates dynamic plasmid repertoires with conserved backbones and diverse accessory modules. We propose that MGE-driven fusion-deletion cycles represent a general principle of plasmid evolution, explaining the rapid emergence and persistence of multidrug-resistant plasmids across bacterial pathogens.
SN  - 2041-1723
SN  - 2041-1723
ER  -