背景回顾：Potassium (K⁺) is an essential element for growth and development in both animals and plants, while high levels of environmental sodium(Na+) represent a threat to most plants. The uptake of K+ from high-saline environments is an essential mechanism to maintain intracellular K+/Na+ homeostasis, which can help reduce toxicity caused by Na+ accumulation, thereby improving the salt tolerance of plants. 

提出问题：However, the mechanisms and regulation of K+-uptake during salt stress remain poorly understood. 

主要发现：In this study, we identified an endoplasmic reticulum–localized cytochrome b5 (OsCYB5-2) that interacted with a high-affinity K+ transporter (OsHAK21) at the plasma membrane. 

结果1-OsCYB5-2与OsHAK21互作，增强后者钾离子转运活性：The association of OsCYB5-2 with the OsHAK21 transporter caused an increase in transporter activity by enhancing the apparent affinity for K+-binding but not Na+-binding. 

结果2-OsHAK21–OsCYB5-2互作调控：Heme binding to OsCYB5-2 was essential for the regulation of OsHAK21. High salinity directly triggered the OsHAK21–OsCYB5-2 interaction, promoting OsHAK21-mediated K+-uptake and restricting Na+ entry into cells; this maintained intracellular K+/Na+ homeostasis in rice cells. 

结果3-OsCYB5-2过表达：Finally, overexpression of OsCYB5-2 increased OsHAK21-mediated K+ transport and improved salt tolerance in rice seedlings. 

结论：This study revealed a posttranslational regulatory mechanism for HAK transporter activity mediated by a cytochrome b₅ and highlighted the coordinated action of two proteins to perceive Na+in response to salt stress.

 摘 要 

钾离子是动物和植物生长和发育中的必要元素，而高水平的环境钠离子浓度对于大多数的植物来水却代表了一种胁迫。从高盐环境中吸收钾离子是维持细胞内钾离子/钠离子内稳态的一个核心机制，能够帮助植物降低由钠离子积累所引起的毒害作用，从而促进植物对于盐胁迫的耐受性。但是，盐胁迫下钾离子吸收的机制及其调控还不清楚。本文中，作者鉴定到了一个定位于内质网的细胞色素b5蛋白OsCYB5-2，该蛋白能够在质膜上与高亲和力钾离子转运蛋白OsHAK21发生互作。OsCYB5-2与OsHAK21转运蛋白的互作通过增强其对于钾离子结合（而非钠离子结合）的表面亲和力，增加转运活性。Heme结合OsCYB5-2对于OsHAK21的调控是非常重要的。高盐浓度会直接诱导OsHAK21–OsCYB5-2互作，促进OsHAK21介导的钾离子吸收，并限制钠离子进入细胞，这维持了水稻细胞中的钾离子/钠离子内稳态。最终，过表达OsCYB5-2基因能够增加OsHAK21介导的钾离子转运，增强水稻幼苗的盐耐受性。本文的研究结果揭示了一个由细胞色素b5蛋白介导的HAK转运活性的翻译后调控机制，并且重点突出了这两个蛋白响应盐胁迫，感知钠离子的协同作用。