Zebin Liu, Qi Niu, Yuxin Dong, Menghao Xu, Jianghao Wu, Lei Gao, Changxin Feng, Yujia Sun, Jiaxuan Zhang, Dongdong Kong, Liangyu Liu, Qifei Gao, Wenzhi Lan, Congcong Hou, Wang Tian, Haiwen Zhang, Zhijie Ren, Sheng Luan, Legong Li
Drought recovery and submergence confer hypoosmotic stress that disrupts plant cellular homeostasis and compromises growth and survival. Although calcium signaling serves as a central hub for plant adaptation to osmotic perturbations, the molecular mechanisms underlying hypoosmotic responses remain poorly understood. In this study, we identified COSR1 (Calcium-permeable Osmotic Stress Response 1) and its homolog COSR2 as Ca2+-permeable channels that are activated by hypoosmotic stimuli. Genetic analyses revealed that COSR1 plays a predominant role, with COSR2 serving a secondary compensatory role, as the cosr1 cosr2 double mutant exhibited substantially more severe phenotypes than either single mutant under post-drought recovery and submergence. Calcium imaging further demonstrated that COSR1 and COSR2 collectively mediate the second spike of hypoosmotic-induced Ca2+ influx, which is closely associated with TCH2/TCH4 induction and stress tolerance. Together, our work establishes that COSR1 and COSR2 are key components of the hypoosmotic-responsive signaling machinery that translates post-drought recovery and submergence-induced osmotic stress into Ca2+ signals, providing novel targets for improving crop resilience.