Koster Maria J E, Timmers H Th Marc
Department of Molecular Cancer Research, Center for Molecular Medicine, University Medical Center Utrecht, 3584 CG, Utrecht, The Netherlands.
Department of Molecular Cancer Research, Center for Molecular Medicine, University Medical Center Utrecht, 3584 CG, Utrecht, The Netherlands
Nucleic Acids Res. 2015 Jan;43(1):143-52. doi: 10.1093/nar/gku1263. Epub 2014 Nov 28.
The activity and dynamic nature of TATA-binding protein (TBP) crucial to RNA polymerase II-mediated transcription is under control of the Mot1p and NC2 complexes. Here we show that both TBP regulatory factors play 'hidden' roles in ensuring transcription fidelity by restricting anti-sense non-coding RNA (ncRNA) synthesis. Production of anti-sense ncRNA transcripts is suppressed by Mot1p- and NC2-mediated release of TBP from binding sites at the 3'-end of genes. In this, Mot1p and NC2 collaborate with the Nrd1p-Nab3p-Sen1p (NNS) complex that terminates the synthesis of anti-sense ncRNAs. In several cases anti-sense ncRNA expression interferes with expression of the cognate sense transcript. Our data reveal a novel regulatory mechanism to suppress anti-sense ncRNA expression and pre-initiation complex (PIC) formation at spurious sites.
对RNA聚合酶II介导的转录至关重要的TATA结合蛋白（TBP）的活性和动态性质受Mot1p和NC2复合物的调控。我们在此表明，这两种TBP调节因子在通过限制反义非编码RNA（ncRNA）合成来确保转录保真度方面发挥着“隐藏”作用。Mot1p和NC2介导TBP从基因3'端的结合位点释放，从而抑制反义ncRNA转录本的产生。在此过程中，Mot1p和NC2与终止反义ncRNA合成的Nrd1p-Nab3p-Sen1p（NNS）复合物协同作用。在几种情况下，反义ncRNA的表达会干扰同源正义转录本的表达。我们的数据揭示了一种抑制反义ncRNA表达以及在假位点形成前起始复合物（PIC）的新型调控机制。
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