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SnRK1 acts upstream of PAP1, contributing to fine-tuning flavonoid biosynthesis in high-light.

上游(联网) 类黄酮 生物合成 类黄酮生物合成 化学 业务 计算机科学 生物化学 电信 基因 转录组 基因表达 抗氧化剂
作者
Josephine Dieckmann,Ralf Stracke,Andreas S. Richter
出处
期刊: [Cold Spring Harbor Laboratory]
标识
DOI:10.1101/2024.06.13.598896
摘要

In land plants, one of the processes vital to cope with environmental changes is the accumulation of photoprotective flavonoids such as flavonols and anthocyanins. The inactivation of SUCROSE NON-FERMENTING1 RELATED PROTEIN KINASE1 (SnRK1), which acts in a chloroplast-derived sugar signalling pathway, permits the activation of flavonoid biosynthesis in high-light. The present study provides genetic evidence that SnRK1 acts upstream of PRODUCTION OF ANTHOCYANIN PIGMENT1 (PAP1), encoding a crucial transcription factor that activates the anthocyanin branch of flavonoid biosynthesis during high-light acclimation. A time-resolved expression analysis indicates a two-step suppression of MYB LIKE2 (MYBL2), a repressor of anthocyanin production, involving SnRK1 inactivation for stable anthocyanin accumulation during prolonged high-light exposure. Furthermore, overexpression of PAP1 resulted in the marked suppression of MYB11, MYB12 and MYB111 and FLAVONOL SYNTHASE1, initiating the flavonol branch of the pathway. Analysis of a flavonoid-deficient CHALCONE SYNTHASE mutant overexpressing PAP1 suggests that regulation of flavonoid biosynthesis is independent of flavonoid intermediates and end products but PAP1-dependent. It is proposed that PAP1 suppresses the flavonol branch by an as yet unknown mechanism, thereby promoting the consumption of carbon building blocks for anthocyanin production to permit the fine-tuning of the pathway.

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