背景回顾：Na⁺ and K+ homeostasis is essential for plant survival in saline soils. A member of the High-Affinity K+ Transporter (HKT) family in rice (Oryza sativa), OsHKT1;1, is a vital regulator of Na+ exclusion from shoots and is bound by a MYB transcription factor (OsMYBc). 

主要发现：Here, we generated transgenic rice lines in the oshkt1;1 mutant background for genetic complementation using genomic OsHKT1;1 containing a native (Com) or mutated (mCom) promoter that cannot be bound by OsMYBc. 

结果1-MYBc：In contrast to wild-type (WT) or Com lines, the mCom lines were not able to recover the salt-sensitive phenotype of oshkt1;1. The OsMYBc-overexpressing plants were more tolerant to salt stress than WT plants. 

结果2-MYBc互作蛋白：A yeast two-hybrid screen using the OsMYBc N terminus as bait identified a rice MYBc stress-related RING finger protein (OsMSRFP). OsMSRFP is an active E3 ligase that ubiquitinated OsMYBc in vitro and mediated 26S proteasome-mediated degradation of OsMYBc under semi-in vitro and in vivo conditions. OsMSRFP attenuated OsMYBc-mediated OsHKT1;1 expression, and knockout of OsMSRFP led to rice salt tolerance. 

结论：These findings uncover a regulatory mechanism of salt response that fine-tunes OsHKT1;1 transcription by ubiquitination of OsMYBc.

 摘 要 

钠离子和钾离子动态平衡对于盐生植物的生存至关重要。水稻HKT家族的OsHKT1;1基因是地上组织Na⁺外排的重要调节器，并能够被MYB转录因子OsMYBc结合。本文中，作者以自身启动子（Com）和一个不能被OsMYBc结合的突变启动子（mCom）驱动OsHKT1;1基因转化oshkt1;1突变体背景株系。与野生型或者Com株系相比，mCom株系不能恢复oshkt1;1突变体的盐敏感表型。OsMYBc过表达植株比野生型植株对盐胁迫的耐受性更强。以OsMYBc蛋白的N末端为诱饵的酵母双杂试验，筛选鉴定出一个水稻MYBc胁迫相关的RING指蛋白OsMSRFP。OsMSRFP是一种具活性的E3连接酶，能够在体外泛素化OsMYBc蛋白，并在体外和体内条件下介导26S蛋白酶体介导的OsMYBc降解。OsMSRFP会减弱OsMYBc介导的OsHKT1;1表达，且OsmSRRFP基因的敲除会导致水稻对盐胁迫具有耐受性。本文的研究结果揭示了一个通过泛素化OsMYBc，精细调控OsHKT1;1基因转录的的盐胁迫调控机制。

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