Low temperature is a major environmental factor that limits plant growth and productivity. Although transient elevation of cytoplasmic calcium has long been recognized as a critical signal for plant cold tolerance, the calcium channels responsible for this process have remained largely elusive. Here we report that OsCNGC9, a cyclic nucleotide-gated channel, positively regulates chilling tolerance by mediating cytoplasmic calcium elevation in rice (Oryza sativa). We showed that the loss-of-function mutant of OsCNGC9 is defective in cold-induced calcium influx and more sensitive to prolonged cold treatment, whereas OsCNGC9 overexpression confers enhanced cold tolerance. Mechanistically, we demonstrated that in response to chilling stress, OsSAPK8, a homolog of Arabidopsis thaliana OST1, phosphorylates and activates OsCNGC9 to trigger Ca²⁺ influx. Moreover, we found that the transcription of OsCNGC9 is activated by a rice dehydration-responsive element-binding transcription factor, OsDREB1A. Taken together, our results suggest that OsCNGC9 enhances chilling tolerance in rice through regulating cold-induced calcium influx and cytoplasmic calcium elevation.

低温是限制植物生长和生产力的主要环境因素。尽管长期以来人们一直认为细胞质钙的瞬时升高是植物耐寒性的关键信号，但造成该过程的钙通道仍然难以捉摸。在这里我们报告说，OsCNGC9，一个环状核苷酸门控通道，通过介导水稻（水稻）中的细胞质钙升高积极调节耐寒性。我们表明，OsCNGC9的功能丧失突变体在冷诱导的钙内流中有缺陷，并且对长时间的冷处理更敏感，而OsCNGC9的过表达赋予增强的耐寒性。从机理上讲，我们证明了在应对寒冷胁迫时，OsSAPK8是拟南芥OST1，磷酸化并激活OsCNGC9以触发Ca ²⁺流入。此外，我们发现OsCNGC9的转录被水稻脱水响应元件结合转录因子OsDREB1A激活。两者合计，我们的结果表明OsCNGC9通过调节冷诱导的钙内流和细胞质钙的升高来增强水稻的耐冷性。