Department of Gene Function and Regulation, Institute of Life Sciences, Chandrasekharpur, Bhubaneswar, Odisha, India.
KTRDC, College of Agriculture-Food and Environment, University of Kentucky, Lexington, KY, 40546, USA.
Planta. 2018 Jan;247(1):181-199. doi: 10.1007/s00425-017-2769-6. Epub 2017 Sep 14.
This paper highlighted a salicylic acid-inducible Caulimoviral promoter fragment from Cestrum yellow leaf curling virus (CmYLCV). Interaction of Arabidopsis transcription factors TGA3 and WRKY53 on CmYLCV promoter resulted in the enhancement of the promoter activity via NPR1-dependent salicylic acid signaling. Several transcriptional promoters isolated from plant-infecting Caulimoviruses are being presently used worldwide as efficient tools for plant gene expression. The CmYLCV promoter has been isolated from the Cestrum yellow leaf curling virus (Caulimoviruses) and characterized more than 12 years ago; also we have earlier reported a near-constitutive, pathogen-inducible CmYLCV promoter fragment (-329 to +137 from transcription start site; TSS) that enhances stronger (3×) expression than the previously reported fragments; all these fragments are highly efficient in monocot and dicot plants (Sahoo et al. Planta 240: 855-875, 2014). Here, we have shown that the full-length CmYLCV promoter fragment (-729 to +137 from TSS) is salicylic acid (SA) inducible. In this context, we have performed an in-depth study to elucidate the factors responsible for SA-inducibility of the CmYLCV promoter. We found that the as-1 and W-box elements (located at -649 and -640 from the TSS) of the CmYLCV promoter are required for SA-induced activation by recruiting Arabidopsis TGA3 and WRKY53 transcription factors. Consequently, as a nascent observation, we established the physical interaction between TGA3 and WYKY53; also demonstrated that the N-terminal domain of TGA3 is sufficient for the interaction with the full-length WRKY53. Such interaction synergistically activates the CmYLCV promoter activity in planta. Further, we found that activation of the CmYLCV promoter by SA through TGA3 and WRKY53 interaction depends on NPR1. Finally, the findings presented here provide strong support for the direct regulatory roles of TGA3 and WRKY53 in the SA and NPR1-dependent activation of a Caulimoviral promoter (CmYLCV).
本文从黄症曲叶病毒（Cestrum yellow leaf curling virus，CmYLCV）中鉴定了一个水杨酸诱导的 caulimovirus 启动子片段。拟南芥转录因子 TGA3 和 WRKY53 与 CmYLCV 启动子相互作用，通过 NPR1 依赖的水杨酸信号增强启动子活性。目前，从侵染植物的 caulimoviruses 中分离出的几种转录启动子被全球广泛用作植物基因表达的有效工具。从黄症曲叶病毒（Caulimoviruses）中分离出 CmYLCV 启动子，并在 12 年前对其进行了特征描述；我们之前还报道了一个近组成型、病原诱导的 CmYLCV 启动子片段（转录起始位点-329 至+137；TSS），该片段的表达增强了 3 倍，优于之前报道的片段；所有这些片段在单子叶植物和双子叶植物中都非常高效（Sahoo 等人，Planta 240：855-875，2014）。在这里，我们表明全长 CmYLCV 启动子片段（TSS 前-729 至+137）可被水杨酸（SA）诱导。在这方面，我们进行了深入研究，以阐明负责 CmYLCV 启动子 SA 诱导的因素。我们发现，CmYLCV 启动子的 as-1 和 W 框元件（位于 TSS 前-649 和-640）对于通过招募拟南芥 TGA3 和 WRKY53 转录因子来诱导 SA 诱导激活是必需的。因此，作为一个新的发现，我们建立了 TGA3 和 WYKY53 之间的物理相互作用；还证明了 TGA3 的 N 端结构域足以与全长 WRKY53 相互作用。这种相互作用协同激活了植物体内的 CmYLCV 启动子活性。此外，我们发现，SA 通过 TGA3 和 WRKY53 相互作用激活 CmYLCV 启动子依赖于 NPR1。最后，本文的研究结果为 TGA3 和 WRKY53 在 SA 和 NPR1 依赖的 Caulimoviral 启动子（CmYLCV）激活中的直接调控作用提供了有力支持。
