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MYB30 和 MYB14 与 WRKY8 形成一个阻遏物-激活物模块,控制葡萄中的芪类生物合成。

MYB30 and MYB14 form a repressor-activator module with WRKY8 that controls stilbene biosynthesis in grapevine.

机构信息

Beijing Key Laboratory of Grape Sciences and Enology, CAS Key Laboratory of Plant Resources, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China.

University of Chinese Academy of Sciences, Beijing 100049, China.

出版信息

Plant Cell. 2023 Jan 2;35(1):552-573. doi: 10.1093/plcell/koac308.

Abstract

When exposed to pathogen infection or ultraviolet (UV) radiation, grapevine (Vitis vinifera) plants rapidly accumulate the stilbenoid resveratrol (Res) with concomitant increase of stilbene synthase (STS), the key enzyme in stilbene biosynthesis. Although a few transcription factors have been shown to regulate STSs, the molecular mechanism governing the regulation of STSs is not well elucidated. Our previous work showed that a VvMYB14-VvWRKY8 regulatory loop fine-tunes stilbene biosynthesis in grapevine through protein-protein interaction; overexpression of VvWRKY8 down-regulates VvMYB14 and VvSTS15/21; and application of exogenous Res up-regulates WRKY8 expression. Here, we identified an R2R3-MYB repressor, VvMYB30, which competes with the activator VvMYB14 for binding to the common binding sites in the VvSTS15/21 promoter. Similar to VvMYB14, VvMYB30 physically interacts with VvWRKY8 through their N-termini, forming a complex that does not bind DNA. Exposure to UV-B/C stress induces VvMYB14, VvWRKY8, and VvSTS15/21, but represses VvMYB30 in grapevine leaves. In addition, MYB30 expression is up-regulated by VvWRKY8-overexpression or exogenous Res. These findings suggest that the VvMYB14-VvWRKY8-VvMYB30 regulatory circuit allows grapevine to respond to UV stress by producing Res and prevents over-accumulation of Res to balance metabolic costs. Our work highlights the stress-mediated induction and feedback inhibition of stilbene biosynthesis through a complex regulatory network involving multiple positive and negative transcriptional regulators.

摘要

当葡萄(Vitis vinifera)植株受到病原体感染或紫外线(UV)辐射时,会迅速积累白藜芦醇(Res),同时伴随着苯丙素合酶(STS)的增加,STS 是苯丙素生物合成的关键酶。虽然已经有几个转录因子被证明可以调节 STS,但 STS 调节的分子机制还没有很好地阐明。我们之前的工作表明,VvMYB14-VvWRKY8 调控环通过蛋白-蛋白相互作用精细调控葡萄中的白藜芦醇生物合成;过表达 VvWRKY8 下调 VvMYB14 和 VvSTS15/21;外源性 Res 的应用上调 WRKY8 的表达。在这里,我们鉴定了一个 R2R3-MYB 抑制剂 VvMYB30,它与激活剂 VvMYB14 竞争结合 VvSTS15/21 启动子上的共同结合位点。与 VvMYB14 相似,VvMYB30 通过其 N 端与 VvWRKY8 物理相互作用,形成一个不结合 DNA 的复合物。UV-B/C 应激诱导 VvMYB14、VvWRKY8 和 VvSTS15/21,但在葡萄叶片中抑制 VvMYB30。此外,MYB30 的表达被 VvWRKY8 的过表达或外源性 Res 上调。这些发现表明,VvMYB14-VvWRKY8-VvMYB30 调控回路允许葡萄通过产生 Res 来应对 UV 应激,并防止 Res 过度积累以平衡代谢成本。我们的工作强调了通过涉及多个正、负转录因子的复杂调控网络,对苯丙素生物合成进行应激诱导和反馈抑制。

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