组蛋白变体 HIS1-3 和 WRKY1 分别正向和负向调控拟南芥的耐盐性。
Linker histone variant HIS1-3 and WRKY1 oppositely regulate salt stress tolerance in Arabidopsis.
机构信息
School of Food and Biological Engineering, Hefei University of Technology, Hefei 230009, China.
School of Horticulture, Anhui Agricultural University, Hefei 230009, China.
出版信息
Plant Physiol. 2022 Jun 27;189(3):1833-1847. doi: 10.1093/plphys/kiac174.
Abstract
The salt overly sensitive (SOS) pathway plays an important role in plant salt stress; however, the transcriptional regulation of the genes in this pathway is unclear. In this study, we found that Linker histone variant HIS1-3 and WRKY1 oppositely regulate the salt stress response in Arabidopsis (Arabidopsis thaliana) through the transcriptional regulation of SOS genes. The expression of HIS1-3 was inhibited by salt stress, and the disruption of HIS1-3 resulted in enhanced salt tolerance. Conversely, the expression of WRKY1 was induced by salt stress, and the loss of WRKY1 function led to increased salt sensitivity. The expression of SOS1, SOS2, and SOS3 was repressed and induced by HIS1-3 and WRKY1, respectively, and HIS1-3 regulated the expression of SOS1 and SOS3 by occupying the WRKY1 binding sites on their promoters. Moreover, WRKY1 and HIS1-3 acted upstream of the SOS pathway. Together, our results indicate that HIS1-3 and WRKY1 oppositely modulate salt tolerance in Arabidopsis through transcriptional regulation of SOS genes.
摘要
盐过度敏感（SOS）途径在植物盐胁迫中起着重要作用；然而，该途径中基因的转录调控尚不清楚。在这项研究中，我们发现组蛋白变体 HIS1-3 和 WRKY1 通过 SOS 基因的转录调控，在拟南芥中对盐胁迫反应起相反的调节作用。盐胁迫抑制 HIS1-3 的表达，而 HIS1-3 的缺失导致盐耐受性增强。相反，WRKY1 的表达被盐胁迫诱导，WRKY1 功能的丧失导致盐敏感性增加。SOS1、SOS2 和 SOS3 的表达分别被 HIS1-3 和 WRKY1 抑制和诱导，并且 HIS1-3 通过占据其启动子上 WRKY1 的结合位点来调节 SOS1 和 SOS3 的表达。此外，WRKY1 和 HIS1-3 在 SOS 途径的上游起作用。总之，我们的研究结果表明，HIS1-3 和 WRKY1 通过 SOS 基因的转录调控，在拟南芥中对盐耐受性起相反的调节作用。
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