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BTB 蛋白 MdBT2 通过触发苹果 MdMYB9 的降解来抑制花色素苷和原花色素生物合成。

BTB protein MdBT2 inhibits anthocyanin and proanthocyanidin biosynthesis by triggering MdMYB9 degradation in apple.

机构信息

State Key Laboratory of Crop Biology, MOA Key Laboratory of Horticultural Crop Biology and Germplasm Innovation, College of Horticulture Science and Engineering, Shandong Agricultural University, Tai-An, Shandong, China.

Research Institute of Pomology, Chinese Academy of Agricultural Sciences, Xingcheng, Liaoning, China.

出版信息

Tree Physiol. 2018 Oct 1;38(10):1578-1587. doi: 10.1093/treephys/tpy063.

DOI:10.1093/treephys/tpy063
PMID:29897546
Abstract

MdMYB9 is a positive regulator in the biosynthesis of anthocyanin and proanthocyanidin in apple. However, its posttranslational regulation is unclear. Here, we demonstrated that the BTB protein MdBT2 had a negative role in the biosynthesis of anthocyanin and proanthocyanidin. MdBT2 interacted with MdMYB9 and negatively regulated the abundance of MdMYB9 protein through the 26S proteasome system. The degradation of MdMYB9 by MdBT2 reduced the expression of MdMYB9-mediated anthocyanin and proanthocyanidin-related genes and reduced the accumulation of anthocyanin and proanthocyanidin, which functioned in an MdCUL3-independent pathway. Our results indicated that MdBT2 negatively regulated the stability of MdMYB9, which provides new insight into the homeostasis of anthocyanin and proanthocyanidin in apple.

摘要

MdMYB9 是苹果花色素苷和原花色素生物合成的正调控因子。然而,其翻译后调控机制尚不清楚。本研究表明,BTB 蛋白 MdBT2 负调控花色素苷和原花色素的生物合成。MdBT2 与 MdMYB9 互作,并通过 26S 蛋白酶体系统负调控 MdMYB9 蛋白的丰度。MdBT2 降解 MdMYB9 降低了 MdMYB9 介导的花色素苷和原花色素相关基因的表达,减少了花色素苷和原花色素的积累,该过程不依赖于 MdCUL3。本研究结果表明,MdBT2 负调控 MdMYB9 的稳定性,为苹果花色素苷和原花色素的内稳态提供了新的见解。

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