Pathogenesis of Plasmopara viticola Depending on Resistance Mediated by Rpv3_1 , and Rpv10 and Rpv3_3 , and by the Vitality of Leaf Tissue

• Published in: Phytopathology 2022-07, Vol.112 (7), p.PHYTO10210415R-1499
• Main Authors: Marie Juraschek, Lena, Matera, Christiane, Steiner, Ulrike, Oerke, Erich-Christian
• Format: Article
• Language: English
• ISSN: 0031-949X; 1943-7684
• DOI: 10.1094/PHYTO-10-21-0415-R

Grapevine cultivars vary in their resistance to , causal agent of downy mildew. Genes from various species confer pathogen resistance ( ), resulting in reduced compatibility of the host-pathogen interaction and partial disease resistance that may become apparent at different stages of pathogenesis. This study describes the pathogenesis of on the partially resistant cultivars Regent ( ) and Solaris ( , ) as compared with the susceptible cultivar Mueller-Thurgau using various microscopic techniques, visual disease rating as well as qPCR. Host plant resistance had no effect on the initial steps of pathogenesis outside the host plant cells (zoospore attachment, formation of substomatal vesicle) and became detectable only after the formation of primary haustoria. The restricted compatibility resulted in reductions in haustorium size and in the number of secondary haustoria and was associated with callose depositions around haustoria and stomatal guard cells, collapsed mesophyll cells (hypersensitive reaction), and additional production of an amorphous substance in the intercellular space of cultivar Solaris. Resistance mechanisms reduced the efficiency of haustoria and largely restricted tissue colonization to the spongy parenchyma; resistance of cultivar Solaris having thicker leaves was more effective than that of cultivar Regent. Despite of the effects of resistance genes, was able to complete its life cycle by forming sporangiophores with sporangia through the stomata on both resistant cultivars indicating partial resistance. Differences in the pathogenesis on detached and attached grapevine leaves highlighted the impact of host tissue vitality on both resistance and susceptibility to the biotrophic pathogen.