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Background  European grapevine cultivars ( Vitis vinifera spp.) are  highly susceptible to the downy mildew pathogen  Plasmopara viticola . Breeding of resistant  V. vinifera  cultivars is a promising strategy to reduce the impact of disease management. Most cultivars that have been bred for resistance to downy mildew, rely on resistance mediated by the  Rpv3  (  R   esistance to    P   .    v   iticola ) locus. However, despite the extensive use of this locus, little is known about the mechanism of  Rpv3 -mediated resistance.    Results  In this study,  Rpv3 -mediated defense responses were investigated in  Rpv3  +  and  Rpv3ˉ  grapevine cultivars following inoculation with two distinct  P. viticola  isolates  avrRpv3  +  and  avrRpv3ˉ , with the latter being able to overcome  Rpv3  resistance. Based on comparative microscopic, metabolomic and transcriptomic analyses, our results show that the  Rpv3–1 -mediated resistance is associated with a defense mechanism that triggers synthesis of fungi-toxic stilbenes and programmed cell death (PCD), resulting in reduced but not suppressed pathogen growth and development. Functional annotation of the encoded protein sequence of genes significantly upregulated during the  Rpv3–1 -mediated defense response revealed putative roles in pathogen recognition, signal transduction and defense responses.    Conclusion  This study used histochemical, transcriptomic and metabolomic analyses of  Rpv3  +  and susceptible cultivars inoculated with avirulent and virulent  P. viticola  isolates to investigate mechanism underlying the  Rpv3–1 -mediated resistance response. We demonstrated a strong correlation between the expressions of stilbene biosynthesis related genes, the accumulation of fungi-toxic stilbenes, pathogen growth inhibition and PCD.    Electronic supplementary material  The online version of this article (10.1186/s12870-019-1935-3) contains supplementary material, which is available to authorized users.

Rpv3–1 mediated resistance to grapevine downy mildew is associated with specific host transcriptional responses and the accumulation of stilbenes