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Resistance to Plasmopara viticola in grapevine ‘Bianca’ is controlled by a major dominant gene causing localised necrosis at the infection site

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Abstract

Downy mildew resistance is a quantitative trait in grapevines of the genus Vitis. The grapevine ‘Bianca’ has retained resistance, originally present in its North American ancestors, through several cycles of backcrossing with susceptible cultivars of Vitis vinifera followed by phenotypic selection. The genetic control of the trait was studied using 116 full-siblings from the cross ‘Chardonnay’ × ‘Bianca’ and parental genetic maps consisting of 298 and 312 markers, respectively. Ratings of resistance and histological identification of the stage of interaction, when pathogen development is impaired in resistant individuals, were performed using leaf disc inoculation assays with two isolates of Plasmopara viticola collected in Italian and French vineyards. ‘Bianca’ and 59% of its offspring were heterozygous for a dominant gene, located in a 2.9 cM interval at the Rpv3 locus on chromosome 18, responsible for the onset of a hypersensitive response (HR) at the infection sites within 2 days post inoculation (dpi). Localised necrosis was the earliest phenotypic difference compared to susceptible individuals, it did not halt pathogen growth, but it was associated with a significant reduction of pathogen performance and disease symptoms from 3 to 6 dpi. QTL peaks for quantitative ratings revealed the strongest effects being caused by the Rpv3 locus: extent of mesophyll colonisation (LOD 3.1, percentage of explained phenotypic variance 16.2%), sporulation density (29.7, 74.3%), and symptom severity expressed by the OIV452 descriptor recommended by the Office International de la Vigne et du Vin (28.3, 74.6%). Strong correlation was observed between the ability of a seedling to mount an HR under controlled experimental conditions and quantitative resistance of the adult plant exposed to natural infections in the field, which was expressed by the number of leaves with fungal sporulation, in two consecutive years of observations.

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Acknowledgments

This research was supported by funds from the Italian Ministry of Agriculture, VIGNA project; from the Italian Ministry of Education and Research PRIN2006 no. 2006073137; from the Regional Government of Friuli Venezia Giulia, Grape Breeding Project; from INRA and the ANR GrapeSeq project. We thank P. Coste, G. Comuzzo, and R. Frezza for technical assistance in plant and inoculum maintenance, D. Copetti for help in field scorings, and C. Coleman for proofreading the manuscript.

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Correspondence to Gabriele Di Gaspero.

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Communicated by M. Xu.

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Supplementary Material S1

– Overview of the experimental design and description of the parameters evaluated in the segregating progeny for describing different components of the resistance trait.(PDF 418 kb)

Supplementary Material S2

– Rainfall (red line expressed in mm), air temperature (minimum, mean, and maximum temperatures, black lines expressed in °C), and relative humidity (green line expressed in %) recorded at the site of field evaluation, during the period of the primary infection when downy mildew symptoms in the ‘Chardonnay’ × ‘Bianca’ progeny under natural conditions were observed. Arrows indicate the date when the number of sporulating leaves was recorded for each individual and used for QTL analysis of disease resistance/susceptibility. (JPG 1475 kb)

Supplementary Material S3

– Consensus genetic map obtained from 116 offspring of the cross ‘Chardonnay’ ×’Bianca’. Distances are given in Kosambi cM. Multi-locus markers are identified by the marker name, suffixed by the code of the parent (–CH for ‘Chardonnay’, and –BI for ‘Bianca’), and when necessary, by a letter (–A, and –B) standing for each non-allelic peak (band) segregating from a given parent. (JPG 1606 kb)

Supplementary Material S4

– Details of parental maps used for mapping. (PDF 10 kb)

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Bellin, D., Peressotti, E., Merdinoglu, D. et al. Resistance to Plasmopara viticola in grapevine ‘Bianca’ is controlled by a major dominant gene causing localised necrosis at the infection site. Theor Appl Genet 120, 163–176 (2009). https://doi.org/10.1007/s00122-009-1167-2

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