Self-transcriptional repression of the Arabidopsis NAC transcription factor ATAF2 and its genetic interaction with phytochrome A in modulating seedling photomorphogenesis
Self-transcriptional repression of the Arabidopsis NAC transcription factor ATAF2 and its genetic interaction with phytochrome A in modulating seedling photomorphogenesis
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DOI：
10.1007/s00425-020-03456-5
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发表时间：
2020-09
期刊：
影响因子：
4.3
通讯作者：
Hao Peng;Jessica Phung;Y. Zhai;M. Neff
中科院分区：
文献类型：
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作者：
Hao Peng;Jessica Phung;Y. Zhai;M. Neff
主要结论NAC转录因子ATAF2通过自身启动子结合抑制自身转录。ATAF2基因与昼夜节律调节因子CCA1和光敏色素A相互作用，调节拟南芥幼苗的光形态发生。摘要ataf2 （ANAC081）是一种NAC （NAM、ATAF和CUC）转录因子（TF），参与拟南芥抗病、胁迫耐受性和激素代谢的调控。我们之前报道过ATAF2通过转录抑制油菜素内酯（BR）使细胞色素P450基因bas1 （CYP734A1，前cyp72b1）和sob7 （CYP72C1）失活，以光依赖的方式促进拟南芥下胚轴的生长。低光强度实验表明，光感受器光敏色素A （PHYA）在ataf2调控的光形态发生中可能比光敏色素B （PHYB）和隐色素1 （CRY1）发挥更关键的作用。此外，ATAF2也受生物钟的调节。核心昼夜节律TF circadian CLOCK ASSOCIATED 1 （CCA1）在dna -蛋白和蛋白水平上与ATAF2相互作用，并不同程度地抑制BAS1-和sob7介导的BR分解代谢。在这项研究中，我们发现ATAF2可以结合其自身的启动子作为转录自我抑制因子。这种自我反馈抑制回路是多种昼夜节律调节基因的典型特征。此外，ataf2和cca1协同抑制幼苗光形态发生，这反映在它们的单基因和双基因敲除突变体的光依赖性下胚轴生长分析中。使用ataf2和光感受器（PHYB， cry1和PHYA）敲除突变体进行的类似的影响率反应分析表明，在广泛的光强度范围内，ataf2调节的光形态发生需要PHYA。此外，phyacan的破坏抑制了ataf2功能缺失幼苗在光照下br不敏感的下胚轴生长表型，而在黑暗中则没有。总的来说，我们的研究结果提供了涉及ATAF2、CCA1和PHYA的昼夜节律-光形态发生- br整合节点的遗传相互作用概要。
Main conclusionThe 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 inArabidopsis thaliana.AbstractATAF2 (ANAC081) is a NAC (NAM, ATAF and CUC) transcription factor (TF) that participates in the regulation of disease resistance, stress tolerance and hormone metabolism inArabidopsis thaliana. We previously reported that ATAF2 promotes Arabidopsis hypocotyl growth in a light-dependent manner via transcriptionally suppressing the brassinosteroid (BR)-inactivating cytochrome P450 genesBAS1(CYP734A1, formerlyCYP72B1) andSOB7(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-feedback-suppression loop is a typical feature of multiple circadian-regulated genes. Additionally,ATAF2andCCA1synergistically 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 usingATAF2and photoreceptor (PHYB,CRY1andPHYA) knock-out mutants demonstrate that PHYA is required for ATAF2-regulated photomorphogenesis in a wide range of light intensities. Furthermore, disruption ofPHYAcan suppress the BR-insensitive hypocotyl-growth phenotype ofATAF2loss-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.