MdWRKY40 与 MdMYB1 协同促进伤诱导的花青素生物合成，并经历 MdBT2 介导的降解。
MdWRKY40 promotes wounding-induced anthocyanin biosynthesis in association with MdMYB1 and undergoes MdBT2-mediated degradation.
机构信息
State Key Laboratory of Crop Biology, Shandong Collaborative Innovation Center for Fruit and Vegetable Production with High Quality and Efficiency, College of Horticulture Science and Engineering, Shandong Agricultural University, Tai-An, 271018, Shandong, China.
出版信息
New Phytol. 2019 Oct;224(1):380-395. doi: 10.1111/nph.16008. Epub 2019 Jul 24.
Wounding stress leads to anthocyanin accumulation. However, the underlying molecular mechanism remains elusive. In this study, MdWRKY40 was found to promote wounding-induced anthocyanin biosynthesis in association with MdMYB1 and undergo MdBT2-mediated degradation in apple. We found that MdMYB1, a positive regulator of anthocyanin biosynthesis, was essential for the wounding-induced anthocyanin biosynthesis in apple. MdWRKY40 was identified as an MdMYB1-interacting protein, and enhanced the binding of MdMYB1 to its target genes in response to wounding. We found that MdBT2 interacted physically with MdWRKY40 and was involved in its degradation through the 26S proteasome pathway. Our results demonstrate that MdWRKY40 is a key modulator in the wounding-induced anthocyanin biosynthesis, which provides new insights into the regulation of wounding-induced anthocyanin biosynthesis at both the transcriptional and post-translational levels in apple.
创伤应激导致花青素积累。然而，其潜在的分子机制仍不清楚。在本研究中，发现 MdWRKY40 与 MdMYB1 一起促进了苹果中的创伤诱导花青素生物合成，并经历了 MdBT2 介导的降解。我们发现，花青素生物合成的正调控因子 MdMYB1 是苹果中创伤诱导花青素生物合成所必需的。MdWRKY40 被鉴定为 MdMYB1 的互作蛋白，并在响应创伤时增强了 MdMYB1 与靶基因的结合。我们发现 MdBT2 与 MdWRKY40 相互作用，并通过 26S 蛋白酶体途径参与其降解。我们的研究结果表明，MdWRKY40 是创伤诱导花青素生物合成的关键调节剂，为苹果中创伤诱导花青素生物合成在转录和翻译后水平上的调控提供了新的见解。
Zotero 插件