Variation in host resistance and pathogen selective value in the interaction between Pinus sylvestris and the fungus Crumenulopsis sororia

Abstract

There have been many studies of plant pathogen evolution in systems showing gene-for-gene control of host resistance. However little is known about situations, exemplified by Scots pine, Pinus sylvestris, and its fungal pathogen Crumenulopsis sororia, where variation in host resistance is quantitative. In a field experiment genetically marked isolates of C. sororia from three natural populations were reciprocally inoculated on 1-and 2-year-old branch tissue of P. sylvestris in the three sites from which they had been collected. Quantitative variation in host resistance was measured by comparing the performance of the same inocula on different host populations, individuals and tissues. The selective value of isolates derived from different populations was estimated by comparing the frequency of genotypes in lesion re-isolations with those in the initial inoculum mixtures. Host resistance varied significantly among populations, individuals within populations and between 1-and 2-year-old branch tissue of P. sylvestris. Large differences in the relative selective values of C. sororia isolates from different populations were detected. The selective value of pathogens was independent of the host population on which they were inoculated. However, their selective value did depend on the age of the tissue on which they grew. The implications of these results for modelling evolution in pathogen-host interactions that lack gene-forgene determination of host resistance are discussed.

Hymenoscyphus pseudoalbidus, the causal agent ofEuropean ash dieback

“…Studies of environmental factors associated with needle colonization by C. ferruginosum have been performed, showing, for example, that the fungus was more frequent on the lower part of a mountain ridge (Sieber et al ., ). The pine canker pathogen Crumenulopsis sororia shows a versatile behaviour depending on site conditions, such as elevation, exposure or slope (Hayes et al ., ), and the age of host tissues (Ennos and McConnell, ). A review of studies on the variation in infectivity and aggressiveness of pathogens in wild systems concludes that such variation is ubiquitous in space and time (Tack et al ., ).…”

The Effect of Heterogeneity on Invasion in Spatial Epidemics: From Theory to Experimental Evidence in a Model System

“…The properties of individual hosts, such as contact rate, susceptibility, or infectiousness, can vary across a population as a result of environmental [1], [2], genetic [3] and immunogenetic [4] factors. Such variability is typically difficult to measure empirically, and has been successfully quantified only in a few significant cases, concerning plant [5], animal [6]–[10], and human diseases [6], [7], [11]. Even more important, a few studies [6], [8]–[10], [12] succeeded in addressing a key epidemiological question: what is, if any, the effect of individual variability on the risk of epidemic invasion [13] (that is, the chance that a pathogen, starting from a single or a few infected hosts, will be able to infect a significant proportion of the whole population).…”

Evolutionary dynamics of interactions between plants and their enemies: comparison of herbivorous insects and pathogens

“…While investigating a possible gene‐for‐gene relationship in a conifer–pathogen system, one study instead implicated the influence of plant chemicals on pathogen attack. In this case, researchers found that among‐population differences in the trees and associated pathogens were influenced by multiple genetic loci and that the gene‐for‐gene mechanism was not adequate to explain the evolutionary trajectory of the interaction …”

“…Escape and radiate: conceptual herbivore, empirical herbivore, empirical pathogen, empirical herbivore and pathogen . Gene for gene: conceptual herbivore, empirical herbivore, conceptual pathogen, empirical pathogen, empirical herbivore and pathogen . Geographic mosaic theory: conceptual herbivore, empirical herbivore, empirical pathogen, conceptual herbivore and pathogen, empirical herbivore and pathogen .…”

“…In this case, researchers found that among-population differences in the trees and associated pathogens were influenced by multiple genetic loci and that the gene-for-gene mechanism was not adequate to explain the evolutionary trajectory of the interaction. 85 The geographic mosaic theory of coevolution. We recovered fewer studies that referenced the GMT than studies that referenced gene-for-gene or escape-and-radiate conceptual models.…”