Black Queen Evolution and Trophic Interactions Determine Plasmid Survival after the Disruption of the Conjugation Network
Cairns, J., Koskinen, K., Penttinen, R., Patinen, T., Hartikainen, A., Jokela, R., Ruusulehto, L., Viitamäki, S., Mattila, S., Hiltunen, T., & Jalasvuori, M. (2018). Black Queen Evolution and Trophic Interactions Determine Plasmid Survival after the Disruption of the Conjugation Network. mSystems, 3(5), Article 00104-18. https://doi.org/10.1128/mSystems.00104-18
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mSystemsAuthors
Date
2018Discipline
Solu- ja molekyylibiologiaBiologisten vuorovaikutusten huippututkimusyksikköNanoscience CenterCell and Molecular BiologyCentre of Excellence in Biological Interactions ResearchNanoscience CenterCopyright
© 2018 the Authors
Mobile genetic elements such as conjugative plasmids are responsible for antibiotic resistance phenotypes in many bacterial pathogens. The ability to conjugate, the presence of antibiotics, and ecological interactions all have a notable role in the persistence of plasmids in bacterial populations. Here, we set out to investigate the contribution of these factors when the conjugation network was disturbed by a plasmid-dependent bacteriophage. Phage alone effectively caused the population to lose plasmids, thus rendering them susceptible to antibiotics. Leakiness of the antibiotic resistance mechanism allowing Black Queen evolution (i.e. a “race to the bottom”) was a more significant factor than the antibiotic concentration (lethal vs sublethal) in determining plasmid prevalence. Interestingly, plasmid loss was also prevented by protozoan predation. These results show that outcomes of attempts to resensitize bacterial communities by disrupting the conjugation network are highly dependent on ecological factors and resistance mechanisms.
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American Society for MicrobiologyISSN Search the Publication Forum
2379-5077Keywords
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https://converis.jyu.fi/converis/portal/detail/Publication/28677432
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Research Council of FinlandFunding program(s)
Academy Research Fellow, AoFAdditional information about funding
This work was supported by an Academy of Finland grant (no. 106993) and a University of Helsinki grant (no. 490152) to T.H.; by a Finnish Cultural Foundation grant (no. 160149) and by University of Helsinki Doctoral Programme in Microbiology and Biotechnology funding to J.C.; and by Academy of Finland grants (no. 252411 and no. 297049) and a Emil Aaltonen Foundation grant to M.J.License
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