Stimulation of RNA polymerase II transcript cleavage activity contributes to maintain transcriptional fidelity in yeast
Stimulation of RNA polymerase II transcript cleavage activity contributes to maintain transcriptional fidelity in yeast
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DOI：
10.1111/j.1365-2443.2007.01072.x
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发表时间：
2007-05-01
期刊：
影响因子：
2.1
通讯作者：
Sekimizu, Kazuhisa
中科院分区：
文献类型：
--
作者：
Koyama, Hiroshi;Ito, Takahiro;Sekimizu, Kazuhisa
转录延伸因子S-II，也称为TFIIS，刺激RNA聚合酶II固有的新生转录物切割活性。Rpb 9是RNA聚合酶II的一个小亚基，可增强S-II的切割刺激活性。在这里，我们研究了新生转录物切割刺激活性对维持酵母中转录保真度的作用。在酵母中，S-II由DST 1基因编码。DST 1基因的破坏降低了细胞中的转录保真度。DST 1基因中降低S-II切割刺激活性的突变导致细胞中转录保真度降低。RPB 9基因的破坏突变体也具有降低的转录保真度。不能增强S-II切割刺激活性的突变体Rpb 9蛋白的表达未能恢复表型。这些结果表明，S-II和Rpb 9通过刺激RNA聚合酶II固有的切割活性来维持转录保真度。与DST 1基因缺失突变体相比，DST 1和RPB 9双突变体具有更严重的转录保真度缺陷，表明RPB 9通过两种机制维持转录保真度，即增强S-II依赖的切割刺激和S-II非依赖的功能。
The transcription elongation factor S-II, also designated TFIIS, stimulates the nascent transcript cleavage activity intrinsic to RNA polymerase II. Rpb9, a small subunit of RNA polymerase II, enhances the cleavage stimulation activity of S-II. Here, we investigated the role of nascent transcript cleavage stimulation activity on the maintenance of transcriptional fidelity in yeast. In yeast, S-II is encoded by the DST1 gene. Disruption of the DST1 gene decreased transcriptional fidelity in cells. Mutations in the DST1 gene that reduce the S-II cleavage stimulation activity led to decreased transcriptional fidelity in cells. A disruption mutant of the RPB9 gene also had decreased transcriptional fidelity. Expression of mutant Rpb9 proteins that are unable to enhance the S-II cleavage stimulation activity failed to restore the phenotype. These results suggest that both S-II and Rpb9 maintain transcriptional fidelity by stimulating the cleavage activity intrinsic to RNA polymerase II. Also, a DST1 and RPB9 double mutant had more severe transcriptional fidelity defect compared with the DST1 gene deletion mutant, suggesting that Rpb9 maintains transcriptional fidelity via two mechanisms, enhancement of S-II dependent cleavage stimulation and S-II independent function(s).