RNA Polymerase II (RNAPII) transcription termination is regulated by the phosphorylation status of the C-terminal domain (CTD). The phosphatase Rtr1 has been shown to regulate serine 5 phosphorylation on the CTD; however, its role in the regulation of RNAPII termination has not been explored. As a consequence of RTR1 deletion, interactions within the termination machinery and between the termination machinery and RNAPII were altered as quantified by Disruption-Compensation (DisCo) network analysis. Of note, interactions between RNAPII and the cleavage factor IA (CF1A) subunit Pcf11 were reduced in rtr1Δ, whereas interactions with the CTD and RNA-binding termination factor Nrd1 were increased. Globally, rtr1Δ leads to decreases in numerous noncoding RNAs that are linked to the Nrd1, Nab3 and Sen1 (NNS) -dependent RNAPII termination pathway. Genome-wide analysis of RNAPII and Nrd1 occupancy suggests that loss of RTR1 leads to increased termination at noncoding genes. Additionally, premature RNAPII termination increases globally at protein-coding genes with a decrease in RNAPII occupancy occurring just after the peak of Nrd1 recruitment during early elongation. The effects of rtr1Δ on RNA expression levels were lost following deletion of the exosome subunit Rrp6, which works with the NNS complex to rapidly degrade a number of noncoding RNAs following termination. Overall, these data suggest that Rtr1 restricts the NNS-dependent termination pathway in WT cells to prevent premature termination of mRNAs and ncRNAs. Rtr1 facilitates low-level elongation of noncoding transcripts that impact RNAPII interference thereby shaping the transcriptome.

中文翻译：

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RNA聚合酶II CTD磷酸酶Rtr1可微调转录终止。

RNA聚合酶II（RNAPII）转录终止受C末端域（CTD）的磷酸化状态调控。已显示磷酸酶Rtr1调节CTD上的丝氨酸5磷酸化；然而，尚未探讨其在调节RNAPII终止中的作用。RTR1删除的结果是，终止机制内以及终止机制与RNAPII之间的相互作用发生了变化，这通过中断补偿（DisCo）网络分析进行了量化。值得注意的是，rtr1Δ中RNAPII和切割因子IA（CF1A）亚基Pcf11之间的相互作用减少，而与CTD和RNA结合终止因子Nrd1的相互作用增加。在全球范围内，rtr1Δ导致与Nrd1，Nab3和Sen1（NNS）依赖性RNAPII终止途径相关的许多非编码RNA减少。全基因组分析的RNAPII和Nrd1的占有率表明，RTR1的丢失导致非编码基因终止的增加。此外，在蛋白质编码基因处，过早的RNAPII终止在全球范围内增加，而在早期延伸过程中Nrd1募集的高峰期刚过后，RNAPII的占有率就会降低。缺失外泌体亚基Rrp6后，rtr1Δ对RNA表达水平的影响消失了，该外泌体亚基Rrp6与NNS复合物协同作用，可在终止后迅速降解许多非编码RNA。总体而言，这些数据表明Rtr1限制了WT细胞中NNS依赖的终止途径，以防止mRNA和ncRNA的过早终止。Rtr1有助于影响RNAPII干扰的非编码转录本的低水平延伸，从而影响转录组。