Abstract

Understanding how habitat heterogeneity may affect the evolution of plant pathogens is essential to effectively predict new epidemiological landscapes and manage genetic diversity under changing global climatic conditions. In this study, we explore the effects of habitat heterogeneity, as determined by variation in host resistance and local temperature, on the evolution of Zymoseptoria tritici by comparing the aggressiveness development of five Z. tritici populations originated from different parts of the world on two wheat cultivars varying in resistance to the pathogen. Our results show that host resistance plays an important role in the evolution of Z. tritici. The pathogen was under weak, constraining selection on a host with quantitative resistance but under a stronger, directional selection on a susceptible host. This difference is consistent with theoretical expectations that suggest that quantitative resistance may slow down the evolution of pathogens and therefore be more durable. Our results also show that local temperature interacts with host resistance in influencing the evolution of the pathogen. When infecting a susceptible host, aggressiveness development of Z. tritici was negatively correlated to temperatures of the original collection sites, suggesting a trade-off between the pathogen’s abilities of adapting to higher temperature and causing disease and global warming may have a negative effect on the evolution of pathogens. The finding that no such relationship was detected when the pathogen infected the partially resistant cultivars indicates the evolution of pathogens in quantitatively resistant hosts is less influenced by environments than in susceptible hosts.

Highlights

  • Plants and pathogens are engaged in a continuous co-evolutionary battle, with pathogens evolving new approaches to attack plants and plants responding through enhanced protection to prevent or mitigate damage (Zhan et al, 2014, 2015)

  • The main objective of this study was to infer the role of genetic variation, host resistance and temperatures on the evolution of pathogens by comparing: (1) aggressiveness development of Z. tritici from geographic locations varying in thermal conditions: (2) the association between the genetic variation and mean of aggressiveness in Z. tritici; and (3) the amount and spatial distribution of genetic variation in neutral molecular markers and aggressiveness on two wheat cultivars differing in Z. tritici resistance

  • The heritability of aggressiveness in the Z. tritici population originating from a susceptible cultivar in Oregon was 15% [(0.652−0.565)/0.565] higher on the susceptible tester cultivar Greina than that on the moderately resistant Toronit

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Summary

Introduction

Plants and pathogens are engaged in a continuous co-evolutionary battle, with pathogens evolving new approaches to attack plants and plants responding through enhanced protection to prevent or mitigate damage (Zhan et al, 2014, 2015). Evolution of Pathogen Aggressiveness life-history trait resulting from the integrated effect of pathogen colonization, development and reproduction on hosts. It is an overall measurement of pathogen fitness composing of infection efficiency, latent period, sporulation rate, infectious period and lesion size (Pariaud et al, 2009) and plays an important role in host-pathogen co-evolution. Host resistance, through its impact on key biological and ecological stochasticities of pathogens such as survival strategies (Carlsson-Graner and Thrall, 2015), reproductive modes (Zhan et al, 2007) and competitive abilities (Zhan and McDonald, 2013), is believed to be one of most important biotic factors shaping the population and evolutionary structure of pathogens (McDonald and Linde, 2002). In agro-ecosystems, resistance has been widely deployed as an artificial means to “compensate” for the host’s relative slowness to respond in the co-evolutionary “armsrace” with pathogens due to the host’s longer generation time and smaller population size compared to their pathogen adversaries (Greischar and Koskella, 2007; Vos et al, 2009)

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