Abstract
Maximizing the durability of crop disease resistance genes in the face of pathogen evolution is a major challenge in modern agricultural epidemiology. Spatial diversification in the deployment of resistance genes, where susceptible and resistant fields are more closely intermixed, is predicted to drive lower epidemic intensities over evolutionary timescales. This is due to an increase in the strength of dilution effects, caused by pathogen inoculum challenging host tissue to which it is not well-specialized. The factors that interact with and determine the magnitude of this spatial suppressive effect are not currently well understood, however, leading to uncertainty over the pathosystems where such a strategy is most likely to be cost-effective. We model the effect on landscape scale disease dynamics of spatial heterogeneity in the arrangement of fields planted with either susceptible or resistant cultivars, and the way in which this effect depends on the parameters governing the pathosystem of interest. Our multiseason semidiscrete epidemiological model tracks spatial spread of wild-type and resistance-breaking pathogen strains, and incorporates a localized reservoir of inoculum, as well as the effects of within and between field transmission. The pathogen dispersal characteristics, any fitness cost(s) of the resistance-breaking trait, the efficacy of host resistance, and the length of the timeframe of interest all influence the strength of the spatial diversification effect. A key result is that spatial diversification has the strongest beneficial effect at intermediate fitness costs of the resistance-breaking trait, an effect driven by a complex set of nonlinear interactions. On the other hand, however, if the resistance-breaking strain is not fit enough to invade the landscape, then a partially effective resistance gene can result in spatial diversification actually worsening the epidemic. These results allow us to make general predictions of the types of system for which spatial diversification is most likely to be cost-effective, paving the way for potential economic modeling and pathosystem specific evaluation. These results highlight the importance of studying the effect of genetics on landscape scale spatial dynamics within host-pathogen disease systems.[Formula: see text] Copyright © 2020 The Author(s). This is an open access article distributed under the CC BY 4.0 International license.
Highlights
Maximizing the durability of crop disease resistance genes in the face of pathogen evolution is a major challenge in modern agricultural epidemiology
We model the effect on landscape scale disease dynamics of spatial heterogeneity in the arrangement of fields planted with either susceptible or resistant cultivars, and the way in which this effect depends on the parameters governing the pathosystem of interest
The values of the transmission parameters are such that in this case the three transmission routes have an equal contribution to maintaining the epidemic, and the mean proportion of plants infected during a season is 0.5. The rational for this is that such a baseline epidemic, with balanced routes of infection and a moderate epidemic intensity, will be clearly responsive to changes in any of the other parameters we explore in this model
Summary
Maximizing the durability of crop disease resistance genes in the face of pathogen evolution is a major challenge in modern agricultural epidemiology. If the resistance-breaking strain is not fit enough to invade the landscape, a partially effective resistance gene can result in spatial diversification worsening the epidemic These results allow us to make general predictions of the types of system for which spatial diversification is most likely to be cost-effective, paving the way for potential economic modeling and pathosystem specific evaluation. These results highlight the importance of studying the effect of genetics on landscape scale spatial dynamics within host_pathogen disease systems. The interaction between plant disease resistance and corresponding pathogen virulence, defined here as the qualitative ability of a pathogen to infect a host, often takes the form of a gene-for-gene
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
