Stracke Ralf, Turgut-Kara Neslihan, Weisshaar Bernd
Bielefeld University, Chair of Genome Research, 33615 Bielefeld, Germany.
Istanbul University, Faculty of Science, Department of Molecular Biology and Genetics, 34134 Vezneciler, Istanbul, Turkey.
Z Naturforsch C J Biosci. 2017 Jul 14;72(7-8):251-257. doi: 10.1515/znc-2016-0221.
The Arabidopsis thaliana R2R3-MYB transcription factor MYB12 is a light-inducible, flavonol-specific activator of flavonoid biosynthesis. The transactivation activity of the AtMYB12 protein was analyzed using a C-terminal deletion series in a transient A. thaliana protoplast assay with the goal of mapping the activation domain (AD). Although the deletion of the last 46 C-terminal amino acids did not affect the activation capacity, the deletion of the last 98 amino acids almost totally abolished transactivation of two different target promoters. A domain swap experiment using the yeast GAL4 DNA-binding domain revealed that the region from positions 282 to 328 of AtMYB12 was sufficient for transactivation. In contrast to the R2R3-MYB ADs known thus far, that of AtMYB12 is not located at the rearmost C-terminal end of the protein. The AtMYB12 AD is conserved in other experimentally proven R2R3-MYB flavonol regulators from different species.
拟南芥R2R3-MYB转录因子MYB12是一种光诱导的、黄酮醇特异性的类黄酮生物合成激活因子。使用C末端缺失系列在瞬时拟南芥原生质体试验中分析AtMYB12蛋白的反式激活活性，目的是绘制激活域（AD）图谱。虽然最后46个C末端氨基酸的缺失不影响激活能力，但最后98个氨基酸的缺失几乎完全消除了两个不同靶启动子的反式激活。使用酵母GAL4 DNA结合域的结构域交换实验表明，AtMYB12第282至328位的区域足以进行反式激活。与迄今为止已知的R2R3-MYB AD不同，AtMYB12的AD并不位于蛋白质的最末端C末端。AtMYB12 AD在来自不同物种的其他经过实验验证的R2R3-MYB黄酮醇调节因子中是保守的。
