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Ontogenic Resistance to Uncinula necator Varies by Genotype and Tissue Type in a Diverse Collection of Vitis spp.

Berries of grapevine (Vitis spp.) have a limited window of susceptibility to Uncinula necator, the causal agent of grapevine powdery mildew, until the onset of ontogenic resistance approximately 2 to 3 weeks postbloom. This phenomenon has been demonstrated in several cultivars of V. vinifera and in V. labruscana ‘Concord’, which all exhibited a similar duration of susceptibility. To identify genetic variation for ontogenic resistance, we screened a diverse collection of Vitis species and interspecific hybrids maintained in the USDA-ARS cold-hardy Vitis germplasm collection in Geneva, NY. Of the 79 genotypes whose fruit clusters were screened for susceptibility to powdery mildew under field conditions, 50 exhibited a high level of constitutive resistance to powdery mildew and did not develop more than trace levels of disease when inoculated, irrespective of the stage of berry development at inoculation. Twenty-four genotypes exhibited a significant gain of resistance as berries aged. This ontogenic resistance was conserved across four species and several interspecific hybrids of Vitis spp., although the timing of the onset of ontogenic resistance varied by genotype. The mechanism of ontogenic resistance was examined for four genotypes. Similar to previous studies, ontogenic resistance greatly reduced the incidence of successful penetration. Despite the broad conservation of ontogenic resistance across species, one genotype (V. rupestris ‘R-65-44’) remained susceptible past the onset of ripening, over 1 month later than reported previously for V. vinifera and V. labruscana. Variation in the resistance phenotype was observed among the rachis, pedicels, and berries within clusters of the majority of genotypes studied. The genetic variation in ontogenic resistance, in particular the discovery of a genotype in which berries remain susceptible as they mature, will facilitate further study of the inheritance and molecular basis of ontogenic resistance.