Single <i>cis</i> ‐elements in brassinosteroid‐induced upregulated genes are insufficient to recruit both redox states of the <scp>BIL1</scp> / <scp>BZR1 DNA</scp> ‐binding domain
The plant-specific transcription factor BRZ-INSENSITIVE-LONG 1 (BIL1)/BRASSINAZOLE-RESISTANT 1 (BZR1) regulates the growth of Arabidopsis thaliana via brassinosteroid signaling, acting as both a gene repressor and activator. Its upregulation requires environmental cues mediated by PHYTOCHROME INTERACTING FACTOR 4 (PIF4), with oxidative modifications via H<sub>2</sub>O<sub>2</sub> enhancing their interaction. However, the nature of the tripartite complex of cis-elements, BIL1/BZR1, and PIF4 under redox changes remains unclear. Here, we demonstrate that oxidation of the DNA-binding domain (DBD) of BIL1/BZR1 alters its DNA-binding ability. However, single cis-elements enriched in brassinosteroid-induced genes do not support binding of either redox form, nor does BIL1/BZR1 DBD heterodimerize with PIF4 DBD on these elements. These findings highlight the complexity of brassinosteroid transcriptional regulation beyond DNA-binding specificity and redox modifications.
Authors
- Morio Ohtsuka
- Shohei Nosaki (ORCID: https://orcid.org/0000-0001-8493-1299)
- Masaru Tanokura (ORCID: https://orcid.org/0000-0001-5072-2480)
- Takuya Miyakawa (ORCID: https://orcid.org/0000-0001-5957-3549)
- Takeshi Nakano (ORCID: https://orcid.org/0000-0002-3188-7770)
Institutions
- University of Tsukuba (JP)
- Tokyo University of Pharmacy and Life Sciences (JP)
- Kyoto University (JP)
- The University of Tokyo (JP)
Publication Details
- Journal
- FEBS Letters
- Published
- 2025-08-29
- DOI
- https://doi.org/10.1002/1873-3468.70147
- Primary Topic
- Plant Molecular Biology Research
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Japan Agency for Medical Research and Development
- Inamori Foundation
- University of Tsukuba
- High Energy Accelerator Research Organization
- Japan Science Society
- Japan Society for the Promotion of Science
- Japan Science and Technology Agency
- ACT-X