Kentucky bluegrass (Poa pratensis L.), one of the most widely used cool-season turfgrasses around the world, is sensitive to powdery mildew (PM; Blumeria graminis). The PM strain identification and regulation mechanisms of Kentucky bluegrass in response to pathogens still remain unclear. Through morphological and molecular analyses, we identified that the pathogen in Kentucky bluegrass was B. graminis f. sp. poae. The infection of B. graminis led to a reduction of the sclerenchyma area, expansion of vesicular cells and movement of chloroplasts. The infected leaves had significantly lower values in net photosynthesis, stomatal conductance and transpiration rate, maximal quantum yield of PSII photochemistry, photochemical quenching and non-regulated energy dissipation compared to mock-inoculated leaves. Expressions of light-harvesting antenna protein genes LHCA and LHCB and photosynthetic electron transport genes petE and petH decreased significantly in infected leaves. Furthermore, upregulations of genes involved in plant-pathogen interaction, such as HSP90, RBOH, and RPM and downregulations of EDS, RPS and WRKY were observed in infected leaves. The findings may help design a feasible approach to effectively control the PM disease in Kentucky bluegrass and other related perennial grass species.
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