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
DisciplineSolu- ja molekyylibiologiaBiologisten vuorovaikutusten huippututkimusyksikköNanoscience CenterCell and Molecular BiologyCentre of Excellence in Biological Interactions ResearchNanoscience Center
© 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. ...
PublisherAmerican Society for Microbiology
ISSN Search the Publication Forum2379-5077
Dataset(s) related to the publicationhttps://doi.org/10.5061/dryad.10gk660
Publication in research information system
MetadataShow full item record
Related funder(s)Academy of Finland
Funding program(s)Academy Research Fellow, AoF
Additional information about fundingThis 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.
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