Kan Yi, Mu Xiao-Rui, Qu Fangfang, Dai Zhi-An, Gao Jin, Liu Ning-Jing, Li Siqi, Shan Jun-Xiang, Ye Wang-Wei, Dong Nai-Qian, Huang Xiaolan, Yang Yi-Bing, Guo Shuang-Qin, Lei Jie-Jie, Cao Ying-Jie, Zhou Ji-Fu, Li Pengcheng, Wang Jianchuan, Li Yixue, Lin Hong-Xuan, Lin Youshun
State Key Laboratory of Plant Trait Design, CAS Center for Excellence in Molecular Plant Sciences, Shanghai Institute of Plant Physiology and Ecology, Chinese Academy of Sciences, Shanghai 200032, China.
State Key Laboratory of Plant Trait Design, CAS Center for Excellence in Molecular Plant Sciences, Shanghai Institute of Plant Physiology and Ecology, Chinese Academy of Sciences, Shanghai 200032, China; University of the Chinese Academy of Sciences, Beijing 100049, China.
Cell. 2025 Dec 24;188(26):7378-7396.e23. doi: 10.1016/j.cell.2025.11.003. Epub 2025 Dec 2.
Heat stress triggers cell membrane lipid remodeling, yet whether this signals plants to perceive high temperatures and how such physical signals are decoded into biological signals remains unclear. Here, we demonstrate that diacylglycerol kinase 7 (DGK7) responds to heat stress at the plasma membrane, converting diacylglycerol into the second messenger, phosphatidic acid (PA). Subsequently, metal-dependent phosphodiesterase (MdPDE1) senses PA, acquires its activity by binding to PA, and translocates to the nucleus to degrade another second messenger, cyclic adenosine monophosphate (cAMP). MdPDE1 then elicits transcriptional landscape changes via altering cAMP signaling. Furthermore, G protein subunit thermotolerance 2 (TT2) inhibits DGK7 activity by Ser dephosphorylation, blocking MdPDE1 activity and nuclear translocation. Notably, field trials demonstrated the promising applications of this mechanism that confers varying degrees of rice thermotolerance as needed. This study establishes a complete hierarchical thermo-decoding mechanism that opens opportunities for creating customized heat-tolerant crops, aiding in mitigating yield losses from global warming.
