2025-12-04 中国科学院(CAS)
<関連情報>
- https://english.cas.cn/newsroom/cas_media/202512/t20251204_1134647.shtml
- https://www.cell.com/cell/abstract/S0092-8674(25)01252-8
植物における熱感知の段階的な解読機構は脂質リモデリングと核シグナル伝達カスケードを結びつける A stepwise decoding mechanism for heat sensing in plants connects lipid remodeling to a nuclear signaling cascade
Yi Kan ∙ Xiao-Rui Mu ∙ Fangfang Qu, ∙ … ∙ Yixue Li ∙ Hong-Xuan Lin ∙ Youshun Lin
Cell Published:December 2, 2025
DOI:https://doi.org/10.1016/j.cell.2025.11.003
Graphical abstract
Highlights
- DGK7 converts physical heat signals into PA lipid signaling as the first step
- G protein TT2 suppresses PA production by inhibiting DGK7 phosphorylation at Ser477
- MdPDE1 senses PA, moves to the nucleus, and hydrolyzes cAMP for biological heat responses
- Molecular design of the TT2-DGK7-MdPDE1 module enables customized heat-tolerant crops
Summary
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 Ser477 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.
