Abstract

The oomycete, Phytophthora infestans, is one of the most important plant pathogens worldwide. This thesis focuses on the late blight pathogen and its host, potato (Solanum tuberosum), and the interaction between these two organisms. Resistance to P. infestans was evaluated histologically, using leaves of potato cultivars with varying levels of general resistance. Preinfectional events could be ruled out as discriminating factors determining the level of resistance in the cultivars studied. After penetration of the pathogen into the leaf tissue there were significant differences between cultivars in hyphal growth and branching. The biochemical response of the tubers to pathogens, more specifically the accumulation of sesquiterpenoid metabolites and their biological effect on P. infestans was examined. Two unique sesquiterpenoid metabolites were isolated from tubers. The influence on mycelial growth of P. infestans of these compounds and of five naturally occurring plant sesquiterpenoids was tested. The two metabolites, isolated from tubers, induced a slight growth stimulation. All other compounds tested, suppressed the growth of the pathogen. The population structure of P. infestans in one single field in southwest Sweden was analysed with the aim to study the origin of the primary infections. Mitochondrial DNA, mating type and SSR-genotype were used as markers. Some foci were monomorphic for all markers, while other foci displayed a large proportion of unique genotypes. This was taken as evidence that inoculum had come both from tubers and oospores within this field. The dynamics of an epidemic and sexual reproduction of P. infestans was investigated in an experimental field inoculated with six different isolates of the pathogen. Three weeks after inoculation sampling was done. The following year, P. infestans isolates were baited from soil samples taken from the field. Parentage analysis, based on SSR markers, showed that recombinant genotypes from the inoculum isolates were present in the soil samples. These findings demonstrate that oospores produced during a summer epidemic in Sweden can overwinter and cause infection the next year.