Several wild apple accessions (Malus sieversii) from Kazakhstan and two (Malus × soulardii, Malus sylvestris) from other parts of the world are highly resistant to blue mold decay caused by Penicillium expansum. Previous studies on the wound responses of these apples to infection by this fungus suggest multiple mechanisms of resistance including innate immunity. In this study, the phenolic composition of extracts from mature wild apples resistant (GMAL 4317.f, PI 589391, and PI 369855) and susceptible (GMAL 3623.i) to blue mold, as well as the susceptible cultivar "Golden Delicious" (Malus × domestica) were investigated using ultra-high-performance liquid chromatography coupled to diode array detection and high resolution multiple stage mass spectrometry (UHPLC/DAD/HRMS). The metabolomic and quantitative results of this study support the hypothesis of the possible relationship between the phenolic content of wild apples and their resistance to P. expansum. Apple accessions resistant to P. expansum had higher concentrations of procyanidins, dihydrochalocone, flavonols, and hydroxycinnamic acids. Findings from this study may lead to development of the physiological markers of resistance that could be used by breeders in evaluating crosses for resistance to blue mold and may be helpful to further define apple defense mechanism(s) against P. expansum.
Blue mold caused primarily by Penicillium expansum and to a lesser extent other Penicillium spp. is the most destructive disease of stored apples in the US and worldwide. It was recently shown that resistance to blue mold exists in wild apple germplasms, Malus sieversii, from Kazakhstan and in other species from different regions maintained as a collection in Geneva, NY. We initiated studies to determine the durability and the mechanism(s) of resistance to P. expansum in select wild apple accessions. Wound responses (up to 96 h in 24 h intervals), affecting P. expansum infection, and related cytological changes were determined in accessions with varying levels of resistance. In general, the more resistant the accession, the quicker the wound response that prevented the fungus from infecting tissue and causing decay. No decay
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