Colgan J, Wampler S, Manley J L
Department of Biological Sciences, Columbia University, New York, New York 10027.
Nature. 1993 Apr 8;362(6420):549-53. doi: 10.1038/362549a0.
Transcription of messenger RNA-encoding genes in vitro requires many protein factors. Transcription factor IID, possibly with the cooperation of TFIIA, binds to the TATA element of the promoter, forming a complex that can bind TFIIB (refs 6, 7) followed by RNA polymerase II (refs 6, 8) and other factors. One or more of these steps is thought to be facilitated by gene-specific transcriptional activation proteins; this seems to require TFIID-associated auxiliary factors and may involve direct contact between the activator and TFIID and/or TFIIB. If such contact is necessary in vivo, activation might conceivably be blocked by a TFIIB derivative containing the sequences necessary for this interaction, but lacking those necessary for binding to the rest of the transcriptional apparatus, an effect similar to that referred to as squelching or transcriptional interference. Here we show that the activity of the glutamine-rich fushi tarazu activation domain is indeed blocked by truncated TFIIB derivatives in Drosophila Schneider L2 cells, suggesting that it is mediated by interactions with TFIIB.
信使核糖核酸编码基因的体外转录需要许多蛋白质因子。转录因子IID可能在TFIIA的协同作用下，与启动子的TATA元件结合，形成一个能结合TFIIB（参考文献6、7）的复合物，随后结合RNA聚合酶II（参考文献6、8）和其他因子。这些步骤中的一个或多个被认为是由基因特异性转录激活蛋白促进的；这似乎需要与TFIID相关的辅助因子，并且可能涉及激活剂与TFIID和/或TFIIB之间的直接接触。如果这种接触在体内是必需的，那么可以想象，激活可能会被一种TFIIB衍生物阻断，该衍生物含有这种相互作用所需的序列，但缺乏与转录装置其余部分结合所需的序列，这种效应类似于所谓的压制或转录干扰。在这里，我们表明，在果蝇施耐德L2细胞中，富含谷氨酰胺的腹节基因激活域的活性确实被截短的TFIIB衍生物所阻断，这表明它是由与TFIIB的相互作用介导的。
