SummaryPotassium (K+) plays a crucial role as a macronutrient in the growth and development of plants. Studies have definitely determined the vital roles of K+ in response to pathogen invasion. Our previous investigations revealed that rice plants infected with rice grassy stunt virus (RGSV) displayed a reduction in K+ content, but the mechanism by which RGSV infection subverts K+ uptake remains unknown. In this study, we found that overexpression of RGSV P1, a specific viral protein encoded by viral RNA1, results in enhanced sensitivity to low K+ stress and exhibits a significantly lower rate of K+ influx compared to wild‐type rice plants. Further investigation revealed that RGSV P1 interacts with OsCIPK23, an upstream regulator of Shaker K+ channel OsAKT1. Moreover, we found that the P1 protein recruits the OsCIPK23 to the Cajal bodies (CBs). In vivo assays demonstrated that the P1 protein competitively binds to OsCIPK23 with both OsCBL1 and OsAKT1. In the nucleus, the P1 protein enhances the binding of OsCIPK23 to OsCoilin, a homologue of the signature protein of CBs in Arabidopsis, and facilitates their trafficking through these CB structures. Genetic analysis indicates that mutant in oscipk23 suppresses RGSV systemic infection. Conversely, osakt1 mutants exhibited increased sensitivity to RGSV infection. These findings suggest that RGSV P1 hinders the absorption of K+ in rice plants by recruiting the OsCIPK23 to the CB structures. This process potentially promotes virus systemic infection but comes at the expense of inhibiting OsAKT1 activity.

中文翻译：

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与水稻 CIPK23 竞争性结合的病毒蛋白抑制钾吸收并促进水稻病毒全身感染

摘要钾 (K+）作为大量营养素在植物的生长和发育中起着至关重要的作用。研究明确确定了 K 的重要作用+以应对病原体的入侵。我们之前的调查显示，感染水稻草矮化病毒（RGSV）的水稻植株表现出 K 值下降。+内容，但 RGSV 感染颠覆 K 的机制+吸收情况仍然未知。在这项研究中，我们发现 RGSV 的过度表达P1是一种由病毒 RNA1 编码的特定病毒蛋白，可增强对低 K 的敏感性+应力并表现出显着较低的 K 率+与野生型水稻植物相比的流入量。进一步研究表明 RGSV P1 与 Shaker K 上游调节因子 OsCIPK23 相互作用+通道 OsAKT1。此外，我们发现 P1 蛋白将 OsCIPK23 募集到卡哈尔小体 (CB)。体内测定表明，P1 蛋白与 OsCBL1 和 OsAKT1 竞争性结合 OsCIPK23。在细胞核中，P1 蛋白增强 OsCIPK23 与 OsCoilin（拟南芥中 CB 特征蛋白的同源物）的结合，并促进它们通过这些 CB 结构的运输。遗传分析表明，突变体oscipk23抑制 RGSV 全身感染。反过来，奥萨克特1突变体表现出对 RGSV 感染的敏感性增加。这些发现表明 RGSV P1 阻碍 K 的吸收+通过将 OsCIPK23 招募到 CB 结构中，在水稻植物中发挥作用。这一过程可能会促进病毒全身感染，但是以抑制 OsAKT1 活性为代价的。