Yun Se-Hun, Khan Irfan Ullah, Noh Bosl, Noh Yoo-Sun
School of Biological Sciences, Seoul National University, Seoul 08826, Korea.
Research Center for Plant Plasticity, Seoul National University, Seoul 08826, Korea.
Nucleic Acids Res. 2024 Apr 24;52(7):3572-3588. doi: 10.1093/nar/gkae019.
The phytohormone salicylic acid (SA) triggers transcriptional reprogramming that leads to SA-induced immunity in plants. NPR1 is an SA receptor and master transcriptional regulator in SA-triggered transcriptional reprogramming. Despite the indispensable role of NPR1, genome-wide direct targets of NPR1 specific to SA signaling have not been identified. Here, we report INA (functional SA analog)-specific genome-wide targets of Arabidopsis NPR1 in plants expressing GFP-fused NPR1 under its native promoter. Analyses of NPR1-dependently expressed direct NPR1 targets revealed that NPR1 primarily activates genes encoding transcription factors upon INA treatment, triggering transcriptional cascades required for INA-induced transcriptional reprogramming and immunity. We identified genome-wide targets of a histone acetyltransferase, HAC1, including hundreds of co-targets shared with NPR1, and showed that NPR1 and HAC1 regulate INA-induced histone acetylation and expression of a subset of the co-targets. Genomic NPR1 targeting was principally mediated by TGACG-motif binding protein (TGA) transcription factors. Furthermore, a group of NPR1 targets mostly encoding transcriptional regulators was already bound to NPR1 in the basal state and showed more rapid and robust induction than other NPR1 targets upon SA signaling. Thus, our study unveils genome-wide NPR1 targeting, its role in transcriptional reprogramming, and the cooperativity between NPR1, HAC1, and TGAs in INA-induced immunity.
植物激素水杨酸（SA）引发转录重编程，从而导致植物产生SA诱导的免疫反应。NPR1是一种SA受体，也是SA触发的转录重编程中的主要转录调节因子。尽管NPR1具有不可或缺的作用，但尚未确定SA信号传导特有的NPR1全基因组直接靶标。在此，我们报告了在其天然启动子下表达绿色荧光蛋白融合NPR1的植物中拟南芥NPR1的INA（功能性SA类似物）特异性全基因组靶标。对NPR1依赖性表达的直接NPR1靶标的分析表明，NPR1在INA处理后主要激活编码转录因子的基因，触发INA诱导的转录重编程和免疫所需的转录级联反应。我们鉴定了组蛋白乙酰转移酶HAC1的全基因组靶标，包括数百个与NPR1共有的靶标，并表明NPR1和HAC1调节INA诱导的组蛋白乙酰化和一部分共靶标的表达。基因组NPR1靶向主要由TGACG基序结合蛋白（TGA）转录因子介导。此外，一组主要编码转录调节因子的NPR1靶标在基础状态下已与NPR1结合，并且在SA信号传导后比其他NPR1靶标表现出更快、更强的诱导。因此，我们的研究揭示了全基因组NPR1靶向、其在转录重编程中的作用以及NPR1、HAC1和TGA在INA诱导的免疫中的协同作用。
