Lee D K, Horikoshi M, Roeder R G
Laboratory of Biochemistry and Molecular Biology, Rockefeller University, New York, New York 10021.
Cell. 1991 Dec 20;67(6):1241-50. doi: 10.1016/0092-8674(91)90300-n.
TFIID binding in the minor groove of DNA at the TATA element was demonstrated by methylation interference and hydroxyl radical footprinting assays, and by binding studies with thymine analog substituted oligonucleotides. These results provide an explanation for TFIID-dependent DNA bending at the TATA element. TFIID binding shows phosphate contacts with the same residues that were found to be essential for TFIID interactions by methylation and thymine-specific modification interference assays. Based on previous studies implicating residues conserved between the direct repeats in DNA binding, as well as models of prokaryotic DNA binding proteins, these results also suggest a model in which the direct repeats of TFIID form two basic antiparallel beta ribbon arms that could contact DNA through the minor groove.
通过甲基化干扰和羟自由基足迹分析，以及与胸腺嘧啶类似物取代的寡核苷酸的结合研究，证实了TFIID在TATA元件处与DNA小沟的结合。这些结果为TATA元件处TFIID依赖性DNA弯曲提供了解释。TFIID结合显示与甲基化和胸腺嘧啶特异性修饰干扰分析中发现对TFIID相互作用至关重要的相同残基存在磷酸接触。基于先前涉及DNA结合中直接重复序列之间保守残基的研究以及原核DNA结合蛋白的模型，这些结果还提出了一个模型，其中TFIID的直接重复序列形成两个基本的反平行β折叠臂，可通过小沟与DNA接触。
