Author:
Zhang Yujuan,Dong Wenke,Zhao Chunxu,Ma Huiling
Abstract
Abstract
Background
Poa pratensis is one of the most common cold-season turfgrasses used for urban turf building, and it is also widely used in ecological environment management worldwide. Powdery mildew is a common disease of P. pratensis. To scientifically and ecologically control lawn powdery mildew, the molecular mechanism underlying the response of P. pratensis to powdery mildew infection must better understood.
Results
To explore molecular mechanism underlying the response of P. pratensis to powdery mildew infection, this study compared physiological changes and transcriptomic level differences between the highly resistant variety ‘BlackJack’ and the extremely susceptible variety ‘EverGlade’ under powdery mildew infection conditions. We analyzed DEGs using reference canonical pathways in the Kyoto Encyclopedia of Genes and Genomes (KEGG) database, and the results showed that “starch and sucrose metabolism”, “photosynthesis” and “fatty acid metabolism”pathways were only enriched in ‘BlackJack’, and the expression of DEGs such as HXK, INV, GS, SS, AGpase and β-amylase in “starch and sucrose metabolism” pathway of ‘BlackJack’ were closely related to powdery mildew resistance. Meanwhile, compared with ‘EverGlade’, powdery mildew infection promoted synthesis of sucrose, expression of photosynthesis parameters and photosynthesis-related enzymes in leaves of ‘BlackJack’ and decreased accumulation of monosaccharides such as glucose and fructose.
Conclusions
This study identified the key metabolic pathways of a P. pratensis variety with high resistance to powdery mildew infection and explored the differences in physiological characteristics and key genes related to sugar metabolism pathways under powdery mildew stress. These findings provide important insights for studying underlying molecular response mechanism.
Funder
Scientific Research Start-up Funds for Openly-recruited Doctors of Gansu Agricultural University
Publisher
Springer Science and Business Media LLC
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