Abstract
BackgroundThe outcome of the arms race between hosts and pathogens depends heavily on the interactions between their genetic diversity, population size and transmission ability. Theory predicts that genetically diverse hosts will select for higher virulence and more diverse pathogens than hosts with low genetic diversity. Cultivated hosts typically have lower genetic diversity and thus small effective population sizes, but can potentially harbour large pathogen population sizes. On the other hand, hosts, such as weeds, which are genetically more diverse and thus have larger effective population sizes, usually harbour smaller pathogen population sizes. Large pathogen population sizes may lead to more opportunities for mutation and hence more diverse pathogens. Here we test the predictions that pathogen neutral genetic diversity will increase with large pathogen population sizes and host diversity, whereas diversity under selection will increase with host diversity. We assessed and compared the diversity of a fungal pathogen, Rhynchosporium commune, on weedy barley grass (which have a large effective population size) and cultivated barley (low genetic diversity) using microsatellites, effector locus nip1 diversity and pathogen aggressiveness in order to assess the importance of weeds in the evolution of the neutral and selected diversity of pathogens.ResultsThe findings indicated that the large barley acreage and low host diversity maintains higher pathogen neutral genetic diversity and lower linkage disequilibrium, while the weed maintains more pathotypes and higher virulence diversity at nip1. Strong evidence for more pathogen migration from barley grass to barley suggests transmission of virulence from barley grass to barley is common.ConclusionsPathogen census population size is a better predictor for neutral genetic diversity than host diversity. Despite maintaining a smaller pathogen census population size, barley grass acts as an important ancillary host to R. commune, harbouring highly virulent pathogen types capable of transmission to barley. Management of disease on crops must therefore include management of weedy ancillary hosts, which may harbour disproportionate supplies of virulent pathogen strains.Electronic supplementary materialThe online version of this article (doi:10.1186/s12862-016-0680-6) contains supplementary material, which is available to authorized users.
Highlights
The outcome of the arms race between hosts and pathogens depends heavily on the interactions between their genetic diversity, population size and transmission ability
We explore the relationships between pathogen and host genetic diversity and population size, using the well-characterised Rhynchosporium commune – barley pathosystem as model
For R. commune we estimate diversity at both neutral microsatellite loci and for pathogen traits and loci that are predicted to be under selection to answer the following four questions: 1) Does host genetic diversity and/or pathogen N affect pathogen neutral genetic diversity and mode of reproduction? 2) Is there more pathogen migration from the weed to the crop, and if so does this enhance the risk of newly evolved virulent strain transfer to barley? 3) Is pathogen genetic diversity under selection related to host genetic diversity? 4) Are pathogen populations from a genetically diverse host more aggressive/virulent than those from a monoculture crop? In our discussion we explore the implications of our improved understanding of the evolutionary processes affecting pathogen diversity
Summary
The outcome of the arms race between hosts and pathogens depends heavily on the interactions between their genetic diversity, population size and transmission ability. Cultivated hosts typically have lower genetic diversity and small effective population sizes, but can potentially harbour large pathogen population sizes. We assessed and compared the diversity of a fungal pathogen, Rhynchosporium commune, on weedy barley grass (which have a large effective population size) and cultivated barley (low genetic diversity) using microsatellites, effector locus nip diversity and pathogen aggressiveness in order to assess the importance of weeds in the evolution of the neutral and selected diversity of pathogens. Variation in host resistance is likely to be of central importance for influencing the patterns of disease incidence and prevalence [15]. It follows, that in order to understand disease dynamics, host diversity is an important consideration
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