Transcriptome analysis of early downy mildew (Plasmopara viticola) defense in grapevines carrying the Asian resistance locus Rpv10

Abstract

The oomycete Plasmopara viticola (Berk. & Curt.) Berl. & de Toni causes downy mildew, one of the most devastating diseases of grapevine (Vitis vinifera L.). Traditional European grapevine cultivars are highly susceptible to this obligate biotrophic pathogen. Large amounts of fungicides are necessary to protect the grapevine plants and secure harvest. This strong requirement for protective chemicals conflicts with the modern demand for sustainability in agriculture. A significant reduction of chemical protection is possible by generating novel robust grapevine cultivars through resistance breeding. Current grapevine breeding utilizes marker-assisted genetic selection. The aim is to combine diverse resistance loci for durable resistance. Markers tagging various resistance loci were elaborated during the last 10 years. However, knowledge about the conveyed defense mechanisms is still sparse but would be essential to optimize the combination of resistance loci. Asian Vitis amurensis accessions carry resistance against downy mildew e.g. in the Rpv10 locus. This locus has been introgressed into the resistant grapevine cultivar ‘Solaris’ and was genetically mapped to chromosome nine. To understand its mode of action in early defense reactions we performed a comparative RNA sequencing analysis after pathogen challenge of Rpv10-carriers, Rpv10-carriers containing additionally the resistance locus Rpv3 from American Vitis sp. origin and non-Rpv carriers. This study indicated comprehensive transcriptional re-programming and a large number of differentially expressed genes. The data indicates that the difference between resistant and susceptible grapevines relies in the increased amount of responsive genes and the efficiency of early signal transduction. This results in the fast activation of large gene clusters encoding phenylalanine ammonium lyase and stilbene synthase on chromosome 16.