Unusually low temperatures caused by global climate change adversely affect rice production. Sensing cold to trigger signal network is a key base for improvement of chilling tolerance trait. Here, we report that Oryza sativa Calreticulin 3 (OsCRT3) localized at the endoplasmic reticulum (ER) exhibits conformational changes under cold stress, thereby enhancing its interaction with CBL-interacting protein kinase 7 (OsCIPK7) to sense cold. Phenotypic analyses of OsCRT3 knock-out mutants and transgenic overexpression lines demonstrate that OsCRT3 is a positive regulator in chilling tolerance. OsCRT3 localizes at the ER and mediates increases in cytosolic calcium levels under cold stress. Notably, cold stress triggers secondary structural changes of OsCRT3 and enhances its binding affinity with OsCIPK7, which finally boosts its kinase activity. Moreover, Calcineurin B-like protein 7 (OsCBL7) and OsCBL8 interact with OsCIPK7 specifically on the plasma membrane. Taken together, our results thus identify a cold-sensing mechanism that simultaneously conveys cold-induced protein conformational change, enhances kinase activity, and Ca²⁺ signal generation to facilitate chilling tolerance in rice.

中文翻译：

---

冷诱导的钙网蛋白 OsCRT3 构象变化促进水稻中 OsCIPK7 结合和温度感应

全球气候变化导致的异常低温对水稻生产产生不利影响。感冷触发信号网络是提高耐寒性状的关键基础。在这里，我们报告定位于内质网 (ER) 的Oryza sativa Calreticulin 3 (OsCRT3) 在冷胁迫下表现出构象变化，从而增强其与 CBL 相互作用蛋白激酶 7 (OsCIPK7) 的相互作用以感知寒冷。OsCRT3表型分析敲除突变体和转基因过表达株系证明 OsCRT3 是耐寒性的正调节因子。OsCRT3 定位于 ER 并介导冷应激下细胞溶质钙水平的增加。值得注意的是，冷应激触发 OsCRT3 的二级结构变化并增强其与 OsCIPK7 的结合亲和力，最终提高其激酶活性。此外，钙调神经磷酸酶 B 样蛋白 7 (OsCBL7) 和 OsCBL8 与质膜上的 OsCIPK7 特异性相互作用。综上所述，我们的结果因此确定了一种冷感应机制，该机制同时传递冷诱导的蛋白质构象变化、增强激酶活性和 Ca ²⁺信号生成，以促进水稻的耐寒性。