No abstract

Kentucky bluegrass (Poa pratensis L.) is a cool-season turfgrass species that responds strongly to nitrogen (N), but the metabolomic responses of this grass species to N supply is unknown. The N-tolerant cultivar Bluemoon and N-sensitive cultivar Balin were exposed to normal N (15 mM) and low N (0.5 mM) for 21 days for identification of differentially expressed metabolites (DEMs) between normal N and low N treatments. Balin had more reductions of chlorophyll and total soluble protein concentrations and a higher accumulation of superoxide radicals under low N stress. A total of 99 known DEMs were identified in either cultivar or both including 22 amino acids and derivatives, 16 carbohydrates, 29 organic acids, and 32 other metabolites. In Bluemoon, β-alanine metabolism was most enriched, followed by alanine, aspartate, and glutamate metabolism, biosynthesis of valine, leucine, and isoleucine biosynthesis, and glycine, serine, and threonine metabolism. In Balin, alanine, aspartate, and glutamate metabolism were most enriched, followed by the tricarboxylic acid (TCA), glyoxylate and decarbohydrate metabolism, and carbon fixation. Bluemoon generally maintained higher TCA cycle capacity and had more downregulated amino acids, while changes in more organic acids occurred in Balin under low N stress. Some metabolite changes by low-N stress were cultivar-specific. The results suggested that regulation of metabolites related to energy production or energy saving could contribute to low N tolerance in Kentucky bluegrass.

Excessive nitrogen (N) application may induce powdery mildew (PM) in perennial grasses, but the resistance mechanisms to PM remain unclear. This study evaluated the physiological and molecular mechanisms of PM resistance affected by N supplies in Kentucky bluegrass (Poa pratensis L.). Cultivar ‘Bluemoon’ (N tolerant) and ‘Balin’ (N sensitive) were treated with low N (0.5 mM), normal N (15 mM), and high N (30 mM) for 21 d in a greenhouse. With increasing N levels, the disease growth was more severe in ‘Balin’ than in ‘Bluemoon’. RNA-seq and weighted gene coexpression network analysis revealed that the PpGS1.1 gene encoding glutamine synthetase was a potential hub gene for PM resistance after comparisons across cultivars and N treatments. The N metabolism pathway was connected with the plant-pathogen interaction pathway via PpGS1.1. The expression of PpGS1.1 in rice protoplasts indicated that the protein was located in the nucleus and cytoplasm. Overexpression of PpGS1.1 in wild type Kentucky bluegrass increased carbon and N contents, and the transgenic plants became more susceptible to PM with a lower wax density. The most differentially expressed genes (DEGs) for N metabolism were upregulated and DEGs for fatty acid metabolism pathway were downregulated in the overexpression lines. The results elucidated mechanisms of PM resistance in relation to N metabolism in Kentucky bluegrass.

No abstract

Artemisia selengensis Turcz. is a valuable edible and medicinal vegetable crop widely cultivated in Northeast China. Powdery mildew (PM) disease occurs during field and greenhouse cultivation, resulting in production losses and quality deterioration. The pathogen in A. selengensis was Golovinomyces artemisiae identified using optical microscopic and scanning electron microscopic observations, morphological identification, and molecular biological analyses. Parameters of chlorophyll fluorescence (ChlF) and antioxidant system responses as well as callose and lignin contents in A. selengensis were analyzed with inoculating G. artemisiae. Obvious of PM-infected leaves were confirmed with significantly lower values in electron transport rate (ETR), non-photochemical quenching (NPQ), photochemical quenching (qP), and actual photochemical efficiency [Y(II)], but higher values in non-adjusting energy dissipation yield [Y(NO)], supposed that maximal photosystem II quantum yield (Fv/Fm) value and images could be used to monitor PM degree on infectedA. selengensis. In addition, malondialdehyde (MDA), superoxide anion (O2–), callose, lignin contents, and peroxidase (POD) activity increased, while superoxide dismutase (SOD) activity, catalase (CAT) activity, and ascorbic acid (AsA) content decreased significantly in infected leaves compared to mock-inoculated leaves, indicated that lignin and protective enzymes are the key indicators for detecting PM resistant in A. selengensis. These results suggest that PM caused by G. artemisiae disrupted the photosynthetic capacity and induced imbalance of antioxidant system inA. selengensis. The findings were of great significance for designing a feasible approach to effectively prevent and control the PM disease in A. selengensis as well as in other vegetable crops.