Abstract Brassinosteroids (BRs) are a group of steroid hormones regulating plant growth and development. Since BRs do not undergo transport among plant tissues, their metabolism is tightly regulated by transcription factors (TFs) and feedback loops. BAS1 (CYP734A1, formerly CYP72B1) and SOB7 (CYP72C1) are two BR-inactivating cytochrome P450s identified in Arabidopsis thaliana. We previously found that a TF ATAF2 (ANAC081) suppresses BAS1 and SOB7 expression by binding to the Evening Element (EE) and CIRCADIAN CLOCK ASSOCIATED 1 (CCA1)-binding site (CBS) on their promoters. Both the EE and CBS are known binding targets of the circadian regulatory protein CCA1. Here, we confirm that CCA1 binds the EE and CBS motifs on BAS1 and SOB7 promoters, respectively. Elevated accumulations of BAS1 and SOB7 transcripts in the CCA1 null mutant cca1-1 indicate that CCA1 is a repressor of their expression. When compared with either cca1-1 or the ATAF2 null mutant ataf2-2, the cca1-1 ataf2-2 double mutant shows higher SOB7 transcript accumulations and a stronger BR-insensitive phenotype of hypocotyl elongation in white light. CCA1 interacts with ATAF2 at both DNA–protein and protein–protein levels. ATAF2, BAS1, and SOB7 are all circadian regulated with distinct expression patterns. These results demonstrate that CCA1 and ATAF2 differentially suppress BAS1- and SOB7-mediated BR inactivation.
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Two ATAF transcription factors ANAC102 and ATAF1 contribute to the suppression of cytochrome P450 ‐mediated brassinosteroid catabolism in Arabidopsis
Abstract PHYB ACTIVATION TAGGED SUPPRESSOR 1 (BAS1) and SUPPRESSOR OF PHYB‐4 7 (SOB7) are two cytochrome P450 enzymes that inactivate brassinosteroids (BRs) inArabidopsis. The NAC transcription factor (TF) ATAF2 (ANAC081) and the core circadian clock regulator CIRCADIAN CLOCK ASSOCIATED 1 (CCA1) both suppress the expression ofBAS1andSOB7via direct promoter binding. Additionally, BRs cause feedback suppression onATAF2expression. Here, we report that two ATAF‐subgroup TFs, ANAC102 and ATAF1 (ANAC002), also contribute to the transcriptional suppression ofBAS1andSOB7.ANAC102andATAF1gene‐knockout mutants exhibit elevated expression of bothBAS1andSOB7, expanded tissue‐level accumulation of their protein products and reduced hypocotyl growth in response to exogenous BR treatments. Similar toATAF2, bothANAC102andATAF1are transcriptionally suppressed by BRs and white light. NeitherBAS1norSOB7expression is further elevated inATAFdouble or triple mutants, suggesting that the suppression effect of these three ATAFs is not additive. In addition,ATAFsingle, double, and triple mutants have similar levels of BR responsiveness with regard to hypocotyl elongation. ATAF2, ANAC102, ATAF1, and CCA1 physically interact with itself and each other, suggesting that they may coordinately suppressBAS1andSOB7expression via protein–protein interactions. Despite the absence of CCA1‐binding elements in their promoters,ANAC102andATAF1have similar transcript circadian oscillation patterns as that ofCCA1, suggesting that these twoATAFgenes may be indirectly regulated by the circadian clock.
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- Award ID(s):
- 1656265
- PAR ID:
- 10450871
- Publisher / Repository:
- Wiley-Blackwell
- Date Published:
- Journal Name:
- Physiologia Plantarum
- Volume:
- 172
- Issue:
- 3
- ISSN:
- 0031-9317
- Page Range / eLocation ID:
- p. 1493-1505
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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