Browse by author
Lookup NU author(s): Dr Tim RudgeORCiD
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
© The Author(s) 2024. Phage predation is generally assumed to reduce microbial proliferation while not contributing to the spread of antibiotic resistance. However, this assumption does not consider the effect of phage predation on the spatial organization of different microbial populations. Here, we show that phage predation can increase the spread of plasmid-encoded antibiotic resistance during surface-associated microbial growth by reshaping spatial organization. Using two strains of the bacterium Escherichia coli, we demonstrate that phage predation slows the spatial segregation of the strains during growth. This increases the number of cell-cell contacts and the extent of conjugation-mediated plasmid transfer between them. The underlying mechanism is that phage predation shifts the location of fastest growth from the biomass periphery to the interior where cells are densely packed and aligned closer to parallel with each other. This creates straighter interfaces between the strains that are less likely to merge together during growth, consequently slowing the spatial segregation of the strains and enhancing plasmid transfer between them. Our results have implications for the design and application of phage therapy and reveal a mechanism for how microbial functions that are deleterious to human and environmental health can proliferate in the absence of positive selection.
Author(s): Ruan C, Ramoneda J, Kan A, Rudge TJ, Wang G, Johnson DR
Publication type: Article
Publication status: Published
Journal: Nature Communications
Year: 2024
Volume: 15
Online publication date: 26/06/2024
Acceptance date: 20/06/2024
Date deposited: 15/07/2024
ISSN (electronic): 2041-1723
Publisher: Springer Nature
URL: https://doi.org/10.1038/s41467-024-49840-7
DOI: 10.1038/s41467-024-49840-7
Data Access Statement: All raw numerical and image data generated in this study have been deposited in the Eawag Research Data Institutional Collection (ERIC) and are freely available to the public at https://doi.org/10.25678/000C1F. Source data are provided with this paper.
PubMed id: 38926498
Altmetrics provided by Altmetric
