Fang Yu, Liao Haicheng, Wei Yingjie, Yin Junjie, Cha Jiankui, Liu Xiaoqian, Chen Xixi, Chen Lin, Ma Zhaotang, Zhang Juan, Yong Shuang, Zhou Xiaogang, Xiong Jun, Cui Xuejia, Lyu Xianju, Li Wei, Zhu He, Yang Yao, Guo Yanbo, Wang Chang, Ouyang Qing, Wang Long, Xiong Qing, Tang Yongyan, Zhu Xiaobo, Lu Xiang, Hou Qingqing, Li Weitao, Chern Mawsheng, He Min, Wang Jing, Song Li, Chen Xuewei
New Cornerstone Science Laboratory, State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Sichuan Agricultural University, Chengdu, Sichuan, China.
Department of Plant Pathology, University of California, Davis, CA, USA.
Nat Commun. 2025 Jul 14;16(1):6485. doi: 10.1038/s41467-025-61827-6.
Global warming impacts crop production and increases crop disease. It is commonly known that heat stress (HS) caused by extreme high temperature induces HS responses but suppresses disease resistance in plants. However, the molecular basis of this trade-off remains largely unknown. Here, we report that OsHsfA4d shows strongest induction upon HS and pathogen infection among Heat Shock Factors (HSFs) in rice. The transcription factor OsHSFA4d enhances thermotolerance by binding to the heat shock element (HSE) in the promoter of HSP101 to activate its expression. OsHSFA4d also binds to the HSE in the first intron of Cellulose synthase-like F6 (CslF6) to promote its expression for suppressing PAMP-triggered ROS bursts and pathogenesis-related gene expression, inhibiting disease resistance. OsCDPK24 and OsCDPK28 interact with OsHSFA4d to form a complex that phosphorylates serine 146 (S146) of OsHSFA4d, thereby enhancing its DNA binding ability. HS induces the kinase activity of OsCDPK24/28 to increase the phosphorylation level of OsHSFA4d. Importantly, residues similar to S146 are conserved in OsHSFA4d orthologues across plant species, suggesting that such phosphorylation modules are widely employed to regulate abiotic and biotic stress responses in the plant kingdom.
全球变暖影响作物产量并增加作物病害。众所周知，极端高温引起的热应激（HS）会诱导植物产生热应激反应，但会抑制植物的抗病性。然而，这种权衡的分子基础在很大程度上仍然未知。在此，我们报道在水稻的热休克因子（HSF）中，OsHsfA4d在热应激和病原体感染时表现出最强的诱导作用。转录因子OsHSFA4d通过与HSP101启动子中的热休克元件（HSE）结合来激活其表达，从而增强耐热性。OsHSFA4d还与类纤维素合酶F6（CslF6）第一个内含子中的HSE结合，以促进其表达，从而抑制由病原体相关分子模式触发的活性氧爆发和病程相关基因的表达，抑制抗病性。OsCDPK24和OsCDPK28与OsHSFA4d相互作用形成复合物，该复合物使OsHSFA4d的丝氨酸146（S146）磷酸化，从而增强其DNA结合能力。热应激诱导OsCDPK24/28的激酶活性，以提高OsHSFA4d的磷酸化水平。重要的是，与S146相似的残基在植物物种的OsHSFA4d直系同源物中是保守的，这表明这种磷酸化模块被广泛用于调节植物界的非生物和生物胁迫反应。
