Self-transcriptional repression of the Arabidopsis NAC transcription factor ATAF2 and its genetic interaction with phyto
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ORIGINAL ARTICLE
Self‑transcriptional repression of the Arabidopsis NAC transcription factor ATAF2 and its genetic interaction with phytochrome A in modulating seedling photomorphogenesis Hao Peng1 · Jessica Phung1 · Ying Zhai2 · Michael M. Neff1 Received: 8 May 2020 / Accepted: 27 August 2020 © Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Main conclusion The NAC transcription factor ATAF2 suppresses its own transcription via self-promoter binding. ATAF2 genetically interacts with the circadian regulator CCA1 and phytochrome A to modulate seedling photomorphogenesis in Arabidopsis thaliana. Abstract ATAF2 (ANAC081) is a NAC (NAM, ATAF and CUC) transcription factor (TF) that participates in the regulation of disease resistance, stress tolerance and hormone metabolism in Arabidopsis thaliana. We previously reported that ATAF2 promotes Arabidopsis hypocotyl growth in a light-dependent manner via transcriptionally suppressing the brassinosteroid (BR)-inactivating cytochrome P450 genes BAS1 (CYP734A1, formerly CYP72B1) and SOB7 (CYP72C1). Assays using low light intensities suggest that the photoreceptor phytochrome A (PHYA) may play a more critical role in ATAF2-regulated photomorphogenesis than phytochrome B (PHYB) and cryptochrome 1 (CRY1). In addition, ATAF2 is also regulated by the circadian clock. The core circadian TF CIRCADIAN CLOCK ASSOCIATED 1 (CCA1) physically interacts with ATAF2 at the DNA–protein and protein–protein levels, and both differentially suppress BAS1- and SOB7-mediated BR catabolism. In this research, we show that ATAF2 can bind its own promoter as a transcriptional self-repressor. This self-feedbacksuppression loop is a typical feature of multiple circadian-regulated genes. Additionally, ATAF2 and CCA1 synergistically suppress seedling photomorphogenesis as reflected by the light-dependent hypocotyl growth analysis of their single and double gene knock-out mutants. Similar fluence-rate response assays using ATAF2 and photoreceptor (PHYB, CRY1 and PHYA) knock-out mutants demonstrate that PHYA is required for ATAF2-regulated photomorphogenesis in a wide range of light intensities. Furthermore, disruption of PHYA can suppress the BR-insensitive hypocotyl-growth phenotype of ATAF2 loss-of-function seedlings in the light, but not in darkness. Collectively, our results provide a genetic interaction synopsis of the circadian-clock-photomorphogenesis-BR integration node involving ATAF2, CCA1 and PHYA. Keywords ATAF2 · Brassinosteroid · CCA1 · Hypocotyl growth · Photomorphogenesis · Phytochrome A
Communicated by Dorothea Bartels. Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00425-020-03456-5) contains supplementary material, which is available to authorized users.
Abbreviations BL Brassinolide BR Brassinosteroid CBS CIRCADIAN CLOCK ASSOCIATED 1-binding site
* Michael M. Neff [email protected]
1
Department of Crop and Soil Sciences, Washington State University, Pullman, WA 99164, USA
Hao Peng [email protected]
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