Max-Planck-Institute for Biophysical Chemistry, Am Fassberg 11, 37077 Göttingen, Germany.
Karolinska Institutet, Department of Biosciences and Nutrition, Center for Innovative Medicine and Science for Life Laboratory, Novum, Hälsovägen 7, 141 83 Huddinge, Sweden.
Mol Cell. 2017 Apr 6;66(1):38-49.e6. doi: 10.1016/j.molcel.2017.02.009. Epub 2017 Mar 16.
At the end of protein-coding genes, RNA polymerase (Pol) II undergoes a concerted transition that involves 3'-processing of the pre-mRNA and transcription termination. Here, we present a genome-wide analysis of the 3'-transition in budding yeast. We find that the 3'-transition globally requires the Pol II elongation factor Spt5 and factors involved in the recognition of the polyadenylation (pA) site and in endonucleolytic RNA cleavage. Pol II release from DNA occurs in a narrow termination window downstream of the pA site and requires the "torpedo" exonuclease Rat1 (XRN2 in human). The Rat1-interacting factor Rai1 contributes to RNA degradation downstream of the pA site. Defects in the 3'-transition can result in increased transcription at downstream genes.
在编码蛋白的基因末端，RNA 聚合酶（Pol）II 经历了一个协同的转变，涉及到前体 mRNA 的 3'加工和转录终止。在这里，我们对芽殖酵母中的 3'转变进行了全基因组分析。我们发现 3'转变全局上需要 Pol II 延伸因子 Spt5 和参与多聚腺苷酸化（pA）位点识别以及内切核酸酶 RNA 切割的因子。Pol II 从 DNA 上的释放发生在 pA 位点下游的一个狭窄的终止窗口中，需要“鱼雷”外切核酸酶 Rat1（人类中的 XRN2）。与 Rat1 相互作用的因子 Rai1 有助于 pA 位点下游的 RNA 降解。3'转变的缺陷可导致下游基因的转录增加。
