Hydrogen peroxide positively regulates brassinosteroid signaling through oxidation of the BRASSINAZOLE-RESISTANT1 transcription factor
Yanchen Tian,
Min Fan,
Zhaoxia Qin,
Hongjun Lv,
Minmin Wang,
Zhe Zhang,
Wenying Zhou,
Na Zhao,
Xiaohui Li,
Chao Han,
Zhaojun Ding,
Wenfei Wang,
Zhi-Yong Wang and
Ming-Yi Bai ()
Additional contact information
Yanchen Tian: Shandong University
Min Fan: Shandong University
Zhaoxia Qin: Shandong University
Hongjun Lv: Shandong University
Minmin Wang: Shandong University
Zhe Zhang: Fujian Agriculture and Forestry University
Wenying Zhou: Shandong University
Na Zhao: Shandong University
Xiaohui Li: Shandong University
Chao Han: Shandong University
Zhaojun Ding: Shandong University
Wenfei Wang: Fujian Agriculture and Forestry University
Zhi-Yong Wang: Carnegie Institution for Science
Ming-Yi Bai: Shandong University
Nature Communications, 2018, vol. 9, issue 1, 1-13
Abstract:
Abstract Hydrogen peroxide (H2O2) is an important signaling molecule in plant developmental processes and stress responses. However, whether H2O2-mediated signaling crosstalks with plant hormone signaling is largely unclear. Here, we show that H2O2 induces the oxidation of the BRASSINAZOLE-RESISTANT1 (BZR1) transcription factor, which functions as a master regulator of brassinosteroid (BR) signaling. Oxidative modification enhances BZR1 transcriptional activity by promoting its interaction with key regulators in the auxin-signaling and light-signaling pathways, including AUXIN RESPONSE FACTOR6 (ARF6) and PHYTOCHROME INTERACTING FACTOR4 (PIF4). Genome-wide analysis shows that H2O2-dependent regulation of BZR1 activity plays a major role in modifying gene expression related to several BR-mediated biological processes. Furthermore, we show that the thioredoxin TRXh5 can interact with BZR1 and catalyzes its reduction. We conclude that reversible oxidation of BZR1 connects H2O2-mediated and thioredoxin-mediated redox signaling to BR signaling to regulate plant development.
Date: 2018
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-03463-x
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DOI: 10.1038/s41467-018-03463-x
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