Transcription factor PnMYC2 positively regulates jasmonate-mediated notoginsenoside biosynthesis in Panax notoginseng

三七 交易激励 生物 转录因子 茉莉酸 细胞生物学 生物合成 茉莉酸甲酯 信号转导 WRKY蛋白质结构域 茉莉酸 抄写(语言学) 抑制因子 调节器 RNA干扰 基因敲除 基因 基因表达 基因表达调控 发起人 心理压抑 生物化学
作者
Jianbin Li,Leilin Li,Jiae Hou,Mingtao Ai,Ruiqi Pu,Tiantai Liu,Huiping Luo,Run Li,Yuan Liu,Ye Yang,Xiuming Cui,Qian Yang
出处
期刊:Horticulture research [Nature Portfolio]
标识
DOI:10.1093/hr/uhag379
摘要

Abstract Notoginsenosides are major bioactive ingredients that directly influence the quality of Panax notoginseng herbs. However, the current understanding of the interplay between environmental signaling and notoginsenoside biosynthesis is limited. Although jasmonates (JAs) are known to regulate the biosynthesis and accumulation of notoginsenosides, the associated signaling pathway remains largely unknown. Here, we identify PnMYC2, a central regulator of JA signaling, as a key node bridging JA signaling to notoginsenoside biosynthesis. Methyl jasmonate (MeJA) treatment markedly induced PnMYC2 expression, accompanied by enhanced notoginsenoside biosynthesis. Further assays revealed that PnMYC2 directly bound the promoters of the PnACAT, PnGGPS, and PnSE, which are involved in notoginsenoside biosynthesis, and activated their expression. Additionally, PnMYC2 also activated the expression of PnLOX5, a JA biosynthetic 13-lipoxygenase gene. Overexpression and interference of PnMYC2 in P. notoginseng calli and leaves indicated that PnMYC2 promoted notoginsenoside and JA biosynthesis by synergistically activating the expression of genes involved in both pathways. Furthermore, MeJA treatment reduced the protein abundance of PnJAZ2 and PnJAZ5, which serve as repressors of JA signaling and interact with PnMYC2 to repress its transactivation activity. Together, our results demonstrate that JAs promote notoginsenoside biosynthesis in P. notoginseng by enhancing the transcription and transactivation activity of PnMYC2. Our findings provide mechanistic insight into the transcriptional mechanism underlying JAs-mediated notoginsenoside biosynthesis.
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