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Data from: Adaptation of the pathogen, Pseudomonas syringae during experimental evolution on a native versus alternative host plant

Citation

Meaden, Sean; Koskella, Britt (2017), Data from: Adaptation of the pathogen, Pseudomonas syringae during experimental evolution on a native versus alternative host plant, Dryad, Dataset, https://doi.org/10.5061/dryad.v444t

Abstract

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 four 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 resequencing 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.

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