Black Rot is a grapevine disease caused by the ascomycete Phyllosticta ampelicida. Neglected so far, this is developing into a pertinent problem in organic viticulture as resistant varieties are still lacking. Here, we follow cellular details of the infection process in the susceptible vinifera variety Müller-Thurgau and screen the ancestral European wild grapevine (V. vinifera sylvestris) for resistance to Black Rot. Using a standardized infection assay, we follow fungal development using LTSEM and quantify key stages on different hosts using fluorescence microscopy. There is considerable variation in susceptibility, which is associated with more rapid leaf maturation. Hyphal growth on different carbon sources shows a preference for pectins over starch, cellulose or xylans. In the resistant sylvestris genotypes Ketsch 16 and Ketsch 18 we find that neither spore attachment nor appressorium formation, but hyphal elongation is significantly inhibited as compared to Müller-Thurgau. Moreover, defence-related oxidative burst and accumulation of phenolic compounds is stimulated in the resistant genotypes. We arrive at a model, where more rapid maturation of the cell wall in these sylvestris genotypes sequesters pectins as major food source and thus block hyphal elongation. This paves the way for introgression of genetic factors responsible for cell wall maturation into V. vinifera to develop Black Rot-resistant varieties of grapevine.
Keywords: Phyllosticta ampelicida; Vitis sylvestris; Black Rot; European Wild Grapevine.
© 2024 The Authors. Plant Biology published by John Wiley & Sons Ltd on behalf of German Society for Plant Sciences, Royal Botanical Society of the Netherlands.