The Rpv3-3 Haplotype and Stilbenoid Induction Mediate Downy Mildew Resistance in a Grapevine Interspecific Population

Abstract

The development of new resistant varieties to the oomycete Plasmopara viticola (Berk.& Curt) is a promising way to combat downy mildew (DM), one of the major diseases threatening the cultivated grapevine (Vitis vinifera L.). Taking advantage of a segregating population derived from “Merzling” (a mid-resistant hybrid) and “Teroldego” (a susceptible landrace), 136 F1 individuals were characterized by combining genetic, phenotypic, and gene expression data to elucidate the genetic basis of DM resistance and polyphenol biosynthesis upon P. viticola infection. An improved consensus linkage map was obtained by scoring 192 microsatellite markers. The progeny were screened for DM resistance and production of 42 polyphenols. QTL mapping showed that DM resistance is associated with the herein named Rpv3-3 specific haplotype and it identified 46 novel metabolic QTLs linked to 30 phenolics-related parameters. A list of the 95 most relevant candidate genes was generated by specifically exploring the stilbenoid-associated QTLs. Expression analysis of 11 genes in Rpv3-3+/− genotypes displaying disparity in DM resistance level and stilbenoid accumulation revealed significant new candidates for the genetic control of stilbenoid biosynthesis and oligomerization. These overall findings emphasized that DM resistance is likely mediated by the major Rpv3-3 haplotype and stilbenoid induction.

Construction of a High-Density Genetic Map and Mapping of Firmness in Grapes (Vitis vinifera L.) Based on Whole-Genome Resequencing

“…The average "Gap < 5 cM" percentage was 99.89%. The average marker distance ranged from 0.59 cM to 1.18 cM, and the map density was higher than other published maps [20,24,26,29]. The linkage map developed in this study possessed good quality and can therefore be used for QTL mapping.…”

“…A (high-density) genetic map is essential for QTL mapping [21]. In the past ten years, a number of grape genetic maps have been constructed based on different mapping populations [20,[22][23][24][25][26][27][28][29][30][31][32][33]. Numerous QTLs for important economic traits, including resistance to downy mildew [10,16,22,[34][35][36][37][38], powdery mildew [34,36,[39][40][41], anthracnose [24], root-knot nematodes [42], and grape phylloxera [43,44], as well as flower sex [45,46], berry color [46,47], seedlessness [48], berry weight [18,32], soluble solid content [32], acidity [20], and muscat flavor [49], have been identified.…”

R-Loci Arrangement Versus Downy and Powdery Mildew Resistance Level: A Vitis Hybrid Survey

“…Rpv3-1 resistance depends on an inducible response specifically elicited by an avirulent strain of P. viticola and is a typical Hypertensive Response (HR), compatible with the cascade of events initiated by the products of NB-LRR and receptor like protein kinase genes, located within the Rpv3-1 locus [35]. Upon the comprehensive study reported by [23], two further wild relative Rpv3 haplotypes have been validated in segregating populations: Rpv3-2 has recently been confirmed by QTL mapping in ‘GF.GA-47-42′ × ‘Villard Blanc’ segregating population [36], while Rpv3-3 has been characterized in a ‘Merzling’ × ‘Teroldego’ progeny [37]. These two haplotypes are less represented in grapevine breeding selections [23] and therefore are novel and valid allelic variants, considering that Rpv3-1 was discovered to be ineffective against a specific P. viticola isolate [19,38].…”

Photosynthetic Cost Associated With Induced Defense to Plasmopara viticola in Grapevine

“…The genomic regions conferring resistance to downy mildew referred to as resistance to P. viticola (Rpv) are quantitatively inherited. To date, 27 quantitative trait loci (QTLs) with major effects on downy mildew resistance are known and described (Fischer et al, 2004;Welter et al, 2007;Bellin et al, 2009;Marguerit et al, 2009;Vezzulli et al, 2019). Rpv1 and Rpv2 are responsible for the resistance derived from Muscadinia rotundifolia (Peressotti et al, 2010) and map to chromosomes 12 and 18, respectively (Merdinoglu et al, 2003;Welter et al, 2007).…”