Adaptation of the pathogen, Pseudomonas syringae, during experimental evolution on a native versus alternative host plant.
© 2017 John Wiley & Sons Ltd. This is an open access article.
The specialization and distribution of pathogens among species has substantial impact on disease spread, especially when reservoir hosts can maintain high pathogen densities or select for increased pathogen virulence. Theory predicts that optimal within-host growth rate will vary among host genotypes/species, and therefore that pathogens infecting multiple hosts should experience different selection pressures depending on the host environment in which they are found. This should be true for pathogens with broad host ranges, but also those experiencing opportunistic infections on novel hosts or that spill over among host populations. There is very little empirical data, however, regarding how adaptation to one host might directly influence infectivity and growth on another. We took an experimental evolution approach to examine short-term adaptation of the plant pathogen, Pseudomonas syringae pathovar tomato, to its native tomato host compared with an alternative host, Arabidopsis, in either the presence or absence of bacteriophages. After 4 serial passages (20 days of selection in planta) we measured bacterial growth of selected lines in leaves of either the focal or alternative host. We found that passage through Arabidopsis led to greater within-host bacterial densities in both hosts than did passage through tomato. Whole genome re-sequencing of evolved isolates identified numerous single nucleotide polymorphisms based on our novel draft assembly for strain PT23. However, there was no clear pattern of clustering among plant selection lines at the genetic level despite the phenotypic differences observed. Together, the results emphasize that previous host associations can influence the within-host growth rate of pathogens. This article is protected by copyright. All rights reserved.
SM was funded by a studentship from the University of Exeter and BK was supported by a NERC research fellowship (NE/K00879X/1). The authors thank Nicole Parr for laboratory support, Gail Preston for donation of the PT23 strain and David Baltrus for genome assembly suggestions.
This is the author accepted manuscript. The final version is available from Wiley via the DOI in this record.
Accepted manuscript online: 16 February 2017
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