Aggressiveness and its role in the adaptation of plant pathogens

International audienceAggressiveness, the quantitative component of pathogenicity, and its role in the adaptation of plant pathogens are still insufficiently investigated. Using mainly examples of biotrophic and necrotrophic fungal pathogens of cereals and Phytophthora infestans on potato, the empirical knowledge on the nature of aggressiveness components and their evolution in response to host and environment is reviewed. Means of measuring aggressiveness components are considered, as well as the sources of environmental variance in these traits. The adaptive potential of aggressiveness components is evaluated by reviewing evidence for their heritability, as well as for constraints on their evolution, including differential interactions between host and pathogen genotypes and trade-offs between components of pathogenicity. Adaptations of pathogen aggressiveness components to host and environment are analysed, showing that: (i) selection for aggressiveness in pathogen populations can be mediated by climatic parameters; (ii) global population changes or remarkable population structures may be explained by variation in aggressiveness; and (iii) selection for quantitative traits can influence pathogen evolution in agricultural pathosystems and can result in differential adaptation to host cultivars, sometimes leading to erosion of quantitative resistance. Possible links with concepts in evolutionary ecology are suggested

Shared influence of pathogen and host genetics on a trade-off between latent period and spore production capacity in the wheat pathogen, Puccinia triticina

Crop pathogens are notorious for their rapid adaptation to their host. We still know little about the evolution of their life cycles and whether there might be trade-offs between fitness components, limiting the evolutionary potential of these pathogens. In this study, we explored a trade-off between spore production capacity and latent period in Puccinia triticina, a fungal pathogen causing leaf rust on wheat. Using a simple multivariate (manova) technique, we showed that the covariance between the two traits is under shared control of host and pathogen, with contributions from host genotype (57%), pathogen genotype (18.4%) and genotypexgenotype interactions (12.5%). We also found variation in sign and strength of genetic correlations for the pathogen, when measured on different host varieties. Our results suggest that these important pathogen life-history traits do not freely respond to directional selection and that precise evolutionary trajectories are contingent on the genetic identity of the interacting host and pathogen