Hong Jeum Kyu, Lee Sung Chul, Hwang Byung Kook
Laboratory of Molecular Plant Pathology, College of Life and Environmental Sciences, Korea University, Anam-dong, Sungbuk-ku, Seoul 136-713, Korea.
Gene. 2005 Aug 15;356:169-80. doi: 10.1016/j.gene.2005.04.030.
The basic PR-1 gene, CABPR1, accumulates in pepper leaf tissues during pathogen infection as well as after ethylene treatment. We isolated and functionally characterized the CABPR1 promoter region in tobacco leaves to identify the cis-acting regulatory sequences that are involved in CABPR1 gene expression. Constructs harboring the 5'-serially deleted CABPR1 promoter, which was fused to the beta-glucuronidase (GUS) gene, were evaluated for their promoter activity in the tobacco leaves. The CABPR1 promoter of 1670 bp in size was locally or systemically induced during a compatible interaction with Pseudomonas syringae pv. tabaci. The CABPR1 promoter also was differentially activated by treatment with ethylene, salicylic acid, nitric oxide, high salinity, drought and low temperature. The expression of the pepper transcription factors, CAZFP1 and CARAV1, activated the CABPR1 promoter. Analyses of a series of 5'-deletions of the CABPR1 promoter indicated that novel cis-acting elements essential for induction by pathogen and abiotic elicitors are localized in the region between -1670 bp and -1466 bp upstream from the translation start site. These results suggest that CABPR1 promoter is essential for regulating CABPR1 gene expression in response to pathogen, abiotic and environmental stresses, possibly by transactivating the CAZFP1 and CARAV1 transcription factors.
基本的病程相关蛋白1(PR-1)基因CABPR1,在病原体感染期间以及乙烯处理后,会在辣椒叶片组织中积累。我们分离并对烟草叶片中的CABPR1启动子区域进行了功能表征,以鉴定参与CABPR1基因表达的顺式作用调控序列。构建了携带与β-葡萄糖醛酸酶(GUS)基因融合的5'端串联缺失CABPR1启动子的载体,并评估其在烟草叶片中的启动子活性。大小为1670 bp的CABPR1启动子在与丁香假单胞菌烟草致病变种的亲和性互作过程中被局部或系统地诱导。CABPR1启动子也会因乙烯、水杨酸、一氧化氮、高盐度、干旱和低温处理而被差异激活。辣椒转录因子CAZFP1和CARAV1的表达激活了CABPR1启动子。对CABPR1启动子一系列5'端缺失的分析表明,病原体和非生物激发子诱导所必需的新型顺式作用元件位于翻译起始位点上游-1670 bp至-1466 bp之间的区域。这些结果表明,CABPR1启动子对于响应病原体、非生物和环境胁迫调节CABPR1基因表达至关重要,可能是通过反式激活CAZFP1和CARAV1转录因子来实现的。