Evolution of pathogenicity, morphological, and genetic traits were analyzed in a local Plasmopara halstedii (downy mildew) population (including two parental and five progeny isolates) multiplied under sunflower qualitative resistance selection pressure for five years. The two components of pathogenicity developed in response to Pl resistance genes selection pressure. The emergence of new virulence in P. halstedii progeny isolates carrying several levels of aggressiveness was an important consequence of selection pressure. However, appearance of new virulence did get along with evolution of aggressiveness in progeny isolates as compared with parental ones. For progeny P. halstedii isolates, an increase in pathogen virulence had direct consequences on its aggressiveness. There was no influence of selection pressure on morphological traits, but an effect was observed on evolution of genetic architecture. However, arrangement of genetic traits did get along with evolution of pathogenicity. It is clear that qualitative resistance selection pressure plays an important role in the evolution of sunflower downy mildew population.
The fast evolution of Plasmopara halstedii (downy mildew) remains a major risk for sunflower crop, as new races of the pathogen are bypassing the resistance of sunflower hybrids. In order to understand the processes which led a new virulence to appear in a local P. halstedii population, the genetic relationships were studied using 12 EST (Expressed Sequence Tag)-derived markers between five progeny isolates of races 300, 304, 314, 704 and 714 and two parental ones of races 100 and 710. All genetic analyses were carried out using five single zoosporangium isolates per P. halstedii isolate. There was no intra-isolate genetic variation among the seven pathogen isolates and five multilocus genotypes (MLG) were identified among the 35 P. halstedii single zoosporangium isolates. The single zoosporangium isolates of races 314, 704 and 714 had an intermediary genetic position between the single zoosporangium isolates of two parental isolates. The single zoosporangium isolates of three isolates of races 100, 300 and 304 were localized in the same genetic clade. Two genetic mechanisms could explain the emergence of new virulence in P. halstedii as a recombination between races and mutations in a clonal lineage.
In order to clarify the role of PlPMI3 resistance gene in sunflower differential lines D4 for differentiation the pathogenicity in Plasmopara halstedii (sunflower downy mildew), analyses were carried out in two groups including four pathotypes which overcome and do not overcome PlPMI3 (Pl gene has still not been mapped) resistance gene. Based on the reaction for the P. halstedii isolates to sunflower hybrids varying only in Pl resistance genes, there were no virulence differences for the two groups. Index of aggressiveness was calculated for pathogen isolates and revealed the presence of significant differences between isolates of races 304 and 314; however, there were no aggressiveness differences for 7xx races. Regarding the life-history trait and the genetic architecture of the pathogen: there were morphological and genetic variations for the four P. halstedii isolates without a correlation with pathogenic diversity. The importance of the PlPMI3 resistance gene to differentiate the pathogenicity in sunflower downy mildew was discussed.