Anthocyanins affect quality in fruits such as grape (Vitis vinifera). High temperatures reduce anthocyanin levels by suppressing the expression of anthocyanin biosynthesis genes and decreasing the biosynthetic rate. However, the regulatory mechanisms that coordinate these two processes remain largely unknown. In this study, we demonstrate that high-temperature-mediated inhibition of anthocyanin biosynthesis in grape berries depends on the auxin and endoplasmic reticulum (ER) stress pathways. Inactivation of these pathways restores anthocyanin accumulation under high temperatures. We identified and characterized FAR-RED ELONGATED HYPOCOTYL3 (FHY3), a high-temperature-modulated transcription factor that activates multiple anthocyanin biosynthesis genes by binding to their promoters. The auxin response factor VvARF3 interacts with VvFHY3 and represses its transactivation activity, antagonizing VvFHY3-induced anthocyanin biosynthesis. Additionally, we found that the ER stress sensor VvbZIP17 represses anthocyanin biosynthesis. VvFHY3 suppresses VvbZIP17 activity by directly binding to the VvbZIP17 promoter to repress its transcription and by physically interacting with VvbZIP17 to block its DNA binding ability. Furthermore, AUXIN RESPONSE FACTOR 3 (ARF3) interferes with the VvFHY3–VvbZIP17 interaction, releasing VvbZIP17 to activate the unfolded protein response and further suppress anthocyanin production. Our results unravel the VvARF3–VvFHY3–VvbZIP17 regulatory module, which links the auxin and ER stress pathways to coordinately repress anthocyanin structural gene expression and biosynthesis under high-temperature stress.

中文翻译：

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VvFHY3 将生长素与内质网应激联系起来，在高温下调节葡萄花青素的生物合成


花青素会影响葡萄 （Vitis vinifera） 等水果的品质。高温通过抑制花青素生物合成基因的表达和降低生物合成速率来降低花青素水平。然而，协调这两个过程的调节机制在很大程度上仍然未知。在这项研究中，我们证明了高温介导的葡萄浆果中花青素生物合成的抑制取决于生长素和内质网 （ER） 胁迫途径。这些途径的失活可恢复高温下的花青素积累。我们鉴定并表征了 FAR-RED ELONGATED HYPOCOTYL3 （FHY3），这是一种高温调节转录因子，通过与启动子结合来激活多个花青素生物合成基因。生长素反应因子 VvARF3 与 VvFHY3 相互作用并抑制其反式激活活性，拮抗 VvFHY3 诱导的花青素生物合成。此外，我们发现 ER 应激传感器 VvbZIP17 抑制花青素的生物合成。VvFHY3 通过直接与 VvbZIP17 启动子结合以抑制其转录，并通过与 VvbZIP17 物理相互作用以阻断其 DNA 结合能力来抑制 VvbZIP17 活性。此外，生长素反应因子 3 （ARF3） 干扰 VvFHY3-VvbZIP17 相互作用，释放 VvbZIP17 以激活未折叠的蛋白质反应并进一步抑制花青素的产生。我们的结果揭示了 VvARF3-VvFHY3-VvbZIP17 调控模块，该模块连接生长素和 ER 胁迫途径，协调抑制高温胁迫下花青素结构基因表达和生物合成。