| Literature DB >> 33278597 |
Jiachang Wang1, Yulong Ren2, Xi Liu3, Sheng Luo2, Xiao Zhang3, Xin Liu2, Qibing Lin2, Shanshan Zhu2, Hua Wan3, Yang Yang4, Yu Zhang3, Bin Lei2, Chunlei Zhou3, Tian Pan3, Yongfei Wang3, Mingming Wu3, Ruonan Jing3, Yang Xu3, Meng Han5, Fuqing Wu2, Cailin Lei2, Xiuping Guo2, Zhijun Cheng2, Xiaoming Zheng2, Yihua Wang3, Zhigang Zhao3, Ling Jiang3, Xin Zhang2, Yong-Fei Wang4, Haiyang Wang2, Jianmin Wan6.
Abstract
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.Entities:
Keywords: OsCNGC9; OsDREB1A; OsSAPK8; chilling tolerance; cold signaling transduction
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Year: 2020 PMID: 33278597 DOI: 10.1016/j.molp.2020.11.022
Source DB: PubMed Journal: Mol Plant ISSN: 1674-2052 Impact factor: 13.164