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Antibiotics as a selective driver for conjugation dynamics

  • Allison J. Lopatkin
  • , Shuqiang Huang
  • , Robert P Smith
  • , Jaydeep K. Srimani
  • , Tatyana A. Sysoeva
  • , Sharon Bewick
  • , David K. Karig
  • , Lingchong You

Research output: Contribution to journal › Article › peer-review

Abstract

It is generally assumed that antibiotics can promote horizontal gene transfer. However, because of a variety of confounding factors that complicate the interpretation of previous studies, the mechanisms by which antibiotics modulate horizontal gene transfer remain poorly understood. In particular, it is unclear whether antibiotics directly regulate the efficiency of horizontal gene transfer, serve as a selection force to modulate population dynamics after such gene transfer has occurred, or both. Here, we address this question by quantifying conjugation dynamics in the presence and absence of antibiotic-mediated selection. Surprisingly, we find that sublethal concentrations of antibiotics from the most widely used classes do not significantly increase the conjugation efficiency. Instead, our modelling and experimental results demonstrate that conjugation dynamics are dictated by antibiotic-mediated selection, which can both promote and suppress conjugation dynamics. Our findings suggest that the contribution of antibiotics to the promotion of horizontal gene transfer may have been overestimated. These findings have implications for designing effective antibiotic treatment protocols and for assessing the risks of antibiotic use.

Original languageAmerican English
Article number16044
JournalNature Microbiology
Volume1
Issue number6
DOIs
StatePublished - Apr 11 2016

Bibliographical note

Publisher Copyright:
© 2016 Macmillan Publishers Limited. All rights reserved.

Funding

The authors acknowledge support from the Shared Materials and Instrumentation Facility at Duke University in assisting with the fabrication of the microfluidic device. The authors also thank T. Dimitriu for plasmid constructs, insightful comments and advice, E. Gullberg for strain DA28102, Y. Feng for pESBL-283, C. Woods for the ESBL library, C. Biesel for plasmid pUA66 and B. Levin, L. David, C. Biesel, K. Koelle, J.C. Kreitz and H.R. Meredith for insightful comments and suggestions. This study was partially supported by the US Army Research Office under grant no. W911NF-14-1-0490 (to D.K., S.B. and L.Y.), the National Institutes of Health (1R01-GM098642, to L.Y.), a David and Lucile Packard Fellowship (to L.Y.) and the Howard G. Clark fellowship (A.J.L.).

FundersFunder number
Howard G. Clark fellowship
National Institutes of Health
National Institute of General Medical SciencesR01GM098642
Army Research OfficeW911NF-14-1-0490

    ASJC Scopus Subject Areas

    • Microbiology
    • Immunology
    • Applied Microbiology and Biotechnology
    • Genetics
    • Microbiology (medical)
    • Cell Biology

    Keywords

    • Antimicrobial resistance
    • Microbiology

    Disciplines

    • Biology
    • Microbiology

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