OsCDPK24 and OsCDPK28 phosphorylate heat shock factor OsHSFA4d to orchestrate abiotic and biotic stress responses in rice

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.

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Publication Details

Journal
Nature Communications
Published
2025-07-14
DOI
https://doi.org/10.1038/s41467-025-61827-6
Citations
11
Primary Topic
Heat shock proteins research
Type
article
Field-Weighted Citation Impact
8.87

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article

OsCDPK24 and OsCDPK28 phosphorylate heat shock factor OsHSFA4d to orchestrate abiotic and biotic stress responses in rice

Xiaobo Zhu, Qingqing Hou, Haicheng Liao, Xuewei Chen et al.
11 citations
Nature Communications
Heat shock proteins research
8.87
article

OsCDPK24 and OsCDPK28 phosphorylate heat shock factor OsHSFA4d to orchestrate abiotic and biotic stress responses in rice

Xiaobo Zhu, Qingqing Hou, Haicheng Liao, Xuewei Chen, He Zhu, Zhaotang Ma, Xuejia Cui, Yongyan Tang, Qing Xiong, Xiang Lu, Xixi Chen, Min He, Yanbo Guo, Shuang Yong, Mawsheng Chern, Wei Li, Chang Wang, Jing Wang, Juan Zhang, Long Wang, Yingjie Wei, Lin Chen, Weitao Li, Xiaoqian Liu, Fang Yu, Jun Xiong, Yang Yao, Xiaogang Zhou, Li Song, Qing Ouyang, X. R. Lyu, Junjie Yin
article en
11 citations

Abstract

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.

Nature CommunicationsVol. 16(1)
Sichuan Agricultural University (CN), University of California, Davis (US)
National Natural Science Foundation of China, Natural Science Foundation of Sichuan Province, National Key Research and Development Program of China, National Cancer Institute
Zero hunger
Openalex Percentile: Top 2%
Heat shock proteins research
8.87
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