LncNAT11-GbMYB11-GbF3’H/GbFLS module mediates flavonol biosynthesis to regulate salt stress tolerance in Ginkgo biloba

银杏 生物合成 黄酮醇 MYB公司 生物化学 类黄酮生物合成 生物 调节器 转录组 转录因子 细胞生物学 类黄酮 基因表达 植物 基因 抗氧化剂
作者
Sian Liu,Hanyue Zhang,Zhaolong Meng,Zhichao Jia,Fangfang Fu,Biao Jin,Fuliang Cao,Li Wang
出处
期刊:Journal of Experimental Botany [Oxford University Press]
标识
DOI:10.1093/jxb/erae438
摘要

Abstract Flavonols are important secondary metabolites that enable plants to resist environmental stresses. Although MYB regulation of flavonol biosynthesis has been well studied, the lncRNA-MYB networks involved in regulating flavonol biosynthesis remain unknown. Ginkgo biloba is rich in flavonols, which are the most important medicinal components. Based on multi-omics data and phylogenetic trees, we identified GbMYB11 as a potential key transcription factor regulating flavonol biosynthesis. Overexpression and VIGS experiments confirmed that GbMYB11 acts as a pivotal positive regulator in flavonol biosynthesis. In the transcriptome of calli overexpressing GbMYB11, we identified significant upregulation of GbF3’H and GbFLS in the flavonol biosynthetic pathway. Yeast one-hybrid and dual-luciferase assays demonstrated that GbMYB11 enhances the expression of GbF3’H and GbFLS by binding to their promoters. Interestingly, we identified LncNAT11, an antisense lncRNA complement to GbMYB11, which negatively regulates flavonol biosynthesis by repressing the expression of GbMYB11. Consequently, we established the LncNAT11-GbMYB11-GbF3’H/GbFLS module as a critical regulator of flavonol biosynthesis in G. biloba, and further elucidated that this module can mitigate the accumulation of reactive oxygen species by modulating flavonol biosynthesis during salt stress. These findings unveil a novel mechanism underlying flavonol biosynthesis and a lncRNA-MYB mediated salt stress tolerance strategy in plants.
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