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Peony Physiological index, interleaf microbial diversity and transcriptome response to Erysiphe paeoniae infection stress

白粉病 生物 转录组 次生代谢 植物 霉病 微生物学 子囊菌纲 从头转录组组装 基因 遗传学 生物合成 基因表达
作者
Xiaojing Liu,Lianrong Feng,Qian Bai,Zhanbin Wang,Muhammad Sabir
出处
期刊:Plant Disease [Scientific Societies]
标识
DOI:10.1094/pdis-09-24-1984-re
摘要

Peony (Paeonia lactiflora Pall.), an important ornamental and medicinal plant, has been severely damaged by the prevalence of powdery mildew, affecting its cultivation and breeding. To ascertain the response mechanism of peony to powdery mildew infection, we examined the microbial diversity, the malondialdehyde (MDA) concentration and antioxidant enzyme activities of mild disease leaves (DL) and healthy leaves (HL) in peony, and transcriptome sequencing in DL and HL was performed. The results showed that the MDA content rose as the degree of infection became worse, while antioxidant enzyme activities increased first and then decreased. Following the occurrance of powdery mildew, fungal community diversity decreased, whereas there was not any significant change in bacterial communities according to microbial diversity sequencing. A total of 1187 differentially expressed genes (DEGs) were obtained from the transcriptome sequencing. Among them, 461 down-regulated DEGs were mainly involved in response to multiple stress factors and protein processing in the endoplasmic reticulum, and 726 up-regulated DEGs were mainly involved in ribosomal structure, sugar metabolism, lipid metabolism, protein translation, and the biosynthesis of terpenoid and polyketides. Furthermore, the pathway involved in plant-pathogen interactions and various disease-resistant transcription factors are crucial in peony defense mechanism against powdery mildew infection. Overall, during the infection of powdery mildew, significant changes occur in the antioxidant capacity and fungal community diversity of peony leaves, while the synthesis of various proteins is also inhibited. In addition, Peony may activate various defense reactions and enhance the biosynthesis of antimicrobial compounds by regulating disease-resistance transcription factors.

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