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Plant Cell|盐胁迫下 DNA 甲基化阅读器-伴侣调节因子-转录因子复合物激活 OsHKT1; 5的表达

灌溉土地日益盐碱化,对农业生产力产生不利影响。为了应对钠离子浓度过高,植物中含有多种钠离子传输系统。水稻(Oryza sativa)高亲钾转运体1; 5(OsHKT1; 5)是一种 Na + 选择性转运体,在盐胁迫下维持 k +/Na + 稳态。然而,调控 OsHKT1; 5表达的机制仍不清楚

在这里,我们提出的证据表明,由水稻 bcl-2相关 ATHANOGENE 4(OsBAG4)、 OsMYB106和 OsSUVH7组成的蛋白复合物调节 OsHKT1; 5在盐胁迫下的表达。我们分离到一个盐胁迫敏感突变体 osbag4-1,该突变体显著降低了 OsHKT1; 5的表达,降低了地上部 k + 和 Na + 水平。利用比较组学法,我们分离出 osbag4相互作用蛋白 ossmyb106(一个 MYB 转录因子)和 OsSUVH7(一个 DNA 甲基化阅读器) ,它们对 OsHKT1; 5的表达至关重要。

Ossmyb106和 OsSUVH7分别结合在 OsHKT1; 5启动子上游的 myb 结合顺式元件(MYBE)和微型反向重复转座子(MITE)上。OsBAG4在 OsSUVH7和 OsMYB106之间起桥梁作用,促进 ossmyb106与 OsHKT1; 5启动子的 MYBE 共识结合,从而激活 OsHKT1; 5的表达。OsHKT1; 5表达减少,盐敏感性增加。

我们的发现揭示了一个转录复合体,包括一个 DNA 甲基化阅读器,一个伴侣调节器,和一个转录因子,协作调节 OsHKT1; 5在盐度胁迫下的表达。

Irrigated lands are increasingly salinized, which adversely affects agricultural productivity. To respond to high sodium (Na+) concentrations, plants harbor multiple Na+-transport systems. Rice (Oryza sativa) HIGH-AFFINITY POTASSIUM (K+) TRANSPORTER 1;5 (OsHKT1;5), a Na+-selective transporter, maintains K+/Na+ homeostasis under salt stress. However, the mechanism regulating OsHKT1;5 expression remains unknown. Here, we present evidence that a protein complex consisting of rice BCL-2-ASSOCIATED ATHANOGENE 4 (OsBAG4), OsMYB106, and OsSUVH7 regulates OsHKT1;5 expression in response to salt stress. We isolated a salt stress-sensitive mutant osbag4-1 that showed significantly reduced OsHKT1;5 expression and reduced K+ and elevated Na+ levels in shoots. Using comparative interactomics, we isolated two OsBAG4-interacting proteins, OsMYB106 (a MYB transcription factor) and OsSUVH7 (a DNA methylation reader) which were crucial for OsHKT1;5 expression. OsMYB106 and OsSUVH7 bound to the MYB-binding cis-element (MYBE) and the miniature inverted-repeat transposable element (MITE) upstream of the MYBE, respectively, in the OsHKT1;5 promoter. OsBAG4 functioned as a bridge between OsSUVH7 and OsMYB106 to facilitate OsMYB106 binding to the consensus MYBE in the OsHKT1;5 promoter, thereby activating the OsHKT1;5 expression. Elimination of the MITE or knockout of OsMYB106 or OsSUVH7 decreased OsHKT1;5 expression and increased salt sensitivity. Our findings reveal a transcriptional complex, consisting of a DNA methylation reader, a chaperone regulator, and a transcription factor, that collaboratively regulate OsHKT1;5 expression during salinity stress.

http://www.plantcell.org/content/plantcell/early/2020/09/15/tpc.20.00301.full.pdf

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