Abstract

Phenotyping trials may not take into account sufficient spatial context to infer quantitative disease resistance of recommended varieties in commercial production settings. Recent ecological theory—the dispersal scaling hypothesis—provides evidence that host heterogeneity and scale of host heterogeneity interact in a predictable and straightforward manner to produce a unimodal (“humpbacked”) distribution of epidemic outcomes. This suggests that the intrinsic artificiality (scale and design) of experimental set-ups may lead to spurious conclusions regarding the resistance of selected elite cultivars, due to the failure of experimental efforts to accurately represent disease pressure in real agricultural situations. In this model-based study we investigate the interaction of host heterogeneity and scale as a confounding factor in the inference from ex-situ assessment of quantitative disease resistance to commercial production settings. We use standard modelling approaches in plant disease epidemiology and a number of different agronomic scenarios. Model results revealed that the interaction of heterogeneity and scale is a determinant of relative varietal performance under epidemic conditions. This is a previously unreported phenomenon that could provide a new basis for informing the design of future phenotyping platforms, and optimising the scale at which quantitative disease resistance is assessed.

Highlights

  • Phenotyping of quantitative disease resistance (QDR) through exposure of plants to pathogens and visual observation of disease symptoms is an important stage in many plant breeding programmes

  • As the results of this study demonstrate, accurate ranking of cultivars or lines according to their relative resistance to disease requires that the level of disease pressure of the designed experiment matches that of the crop in its commercial production setting

  • This study refines and extends new ecological theory by characterising the relationship between host heterogeneity, scale of heterogeneity, and the progress of plant disease epidemics in crop varieties with varying levels of QDR. We conclude that this relationship follows the dispersal scaling hypothesis (DSH), with the proviso that sufficient time has elapsed to promote invasive spread

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Summary

Introduction

Phenotyping of quantitative disease resistance (QDR) through exposure of plants to pathogens and visual observation of disease symptoms is an important stage in many plant breeding programmes. In the field there is a trend towards reducing plot size in order to maximize the number of varieties that can be assessed, such as the use of small unbordered ―hills‖ or spaced plants differing in height and maturity, ear rows or short-rod rows containing only a few seeds, or micro-plots arranged in a matrix [3] In such cases, the phenotyping of QDR may be confounded by the artificial environment (e.g., high temperatures in glasshouses), or complicated by competition effects from neighbours that do not reproduce the competition experienced by plants grown in canopies in the field, or impaired by unnaturally low or high levels of initial or background inoculum

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