JA-induced FtBPM3 accumulation promotes FtERF-EAR3 degradation and rutin biosynthesis in Tartary buckwheat

Buckwheat accumulates abundant flavonoids, which exhibit excellent health-promoting value. Flavonoids biosynthesis is mediated by a variety of phytohormones, among which jasmonates (JAs) induce numerous transcription factors, taking part in regulation of flavonoids biosynthesis genes. However, some transcriptional repressors appeared also induced by JAs. How these transcriptional repressors coordinately participate in JA signaling remains unclear. Here, we found that the disruption of the GCC-box in FtF3H promoter was associated with flavonoids accumulation in Tartary buckwheat. Further, our study illustrated that the nucleus-localized FtERF-EAR3 could inhibit FtF3H expression and flavonoids biosynthesis through binding the GCC-box in the promoter of FtF3H. The JA induced FtERF-EAR3 gene expression while facilitating FtERF-EAR3 protein degradation via the FtBPM3-dependent 26S proteasome pathway. Overall, these results illustrate a precise modulation mechanism of JA-responsive transcription suppressor participating in flavonoid biosynthesis, and will further help to improve the efficiency of flavonoids biosynthesis in Tartary buckwheat.

Automated summary

This study reveals the mechanism of a transcription suppressor, FtERF-EAR3, in regulating flavonoid biosynthesis in Tartary buckwheat. FtERF-EAR3 inhibits FtF3H expression and flavonoid biosynthesis by binding to the GCC-box in the promoter of FtF3H. The gene expression of FtERF-EAR3 is induced by JA and the protein is degraded through the FtBPM3-dependent 26S proteasome pathway. Understanding the regulation mechanism of flavonoid biosynthesis in Tartary buckwheat is significant for improving its production efficiency.