Rat1p maintains RNA polymerase II CTD phosphorylation balance.
Rat1p maintains RNA polymerase II CTD phosphorylation balance.
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DOI：
10.1261/rna.041129.113
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发表时间：
2014-04
期刊：
影响因子：
--
通讯作者：
Jensen TH
中科院分区：
文献类型：
--
作者：
Jimeno-González S;Schmid M;Malagon F;Haaning LL;Jensen TH
酿酒酵母5‘-3’外切酶Rat1p可能通过3‘端切割后下游RNA的降解参与转录终止。本研究表明，RAT1-1突变体表现出RNA聚合酶II C末端结构域的磷酸化和转录延伸率的增加，并且RAT1-1的表型可以被磷酸酶Fcp1p的过度表达所抑制。因此，Rat1p在转录控制中扮演着复杂的角色，在分析Rat1-1突变表型时必须考虑这些作用。在酿酒酵母中，5‘-3’外切酶Rat1p参与转录终止。尽管Rat1p介导的RNA降解被认为对这种活性起作用，但Rat1p帮助从DNA模板中释放RNA聚合酶II(RNAPII)的确切机制尚不清楚。在这里，我们描述了Rat1p在转录延伸过程中调节最大RNAPII亚单位Rpb1p的C-末端结构域(CTD)磷酸化水平的功能。RAT1-1突变体表现出高度的CTD磷酸化水平以及RNAPII分布和转录终止缺陷。这些表型都可以通过CTD磷酸酶Fcp1p的过度表达来挽救，这表明Rat1p活性缺失、CTD磷酸化水平升高和转录缺陷之间存在功能关系。我们还证明RAT1-1细胞表现出增加的RNAPII转录动力学，这一特征可能有助于突变的细胞表型。RAT1-1等位基因与rpb1-E1103G突变是合成致死的，导致RNAPII速度加快，并被rpb2-10突变抑制，导致转录减慢。因此，Rat1p在控制转录方面扮演着比之前认为的更复杂的角色。
The S. cerevisiae 5′-3′ exonuclease Rat1p is supposed to partake in transcription termination via decay of downstream RNA after 3′-end cleavage. This study reveals that rat1-1 mutant displays increased phosphorylation of RNA polymerase II C-terminal domain and transcription elongation rates and that rat1-1 phenotypes can be suppressed by overexpression of the phosphatase Fcp1p. Thus, Rat1p plays complex roles in controlling transcription that have to be considered when analyzing rat1-1 mutant phenotypes. In S. cerevisiae, the 5′-3′ exonuclease Rat1p partakes in transcription termination. Although Rat1p-mediated RNA degradation has been suggested to play a role for this activity, the exact mechanisms by which Rat1p helps release RNA polymerase II (RNAPII) from the DNA template are poorly understood. Here we describe a function of Rat1p in regulating phosphorylation levels of the C-terminal domain (CTD) of the largest RNAPII subunit, Rpb1p, during transcription elongation. The rat1-1 mutant exhibits highly elevated levels of CTD phosphorylation as well as RNAPII distribution and transcription termination defects. These phenotypes are all rescued by overexpression of the CTD phosphatase Fcp1p, suggesting a functional relationship between the absence of Rat1p activity, elevated CTD phosphorylation, and transcription defects. We also demonstrate that rat1-1 cells display increased RNAPII transcription kinetics, a feature that may contribute to the cellular phenotypes of the mutant. Consistently, the rat1-1 allele is synthetic lethal with the rpb1-E1103G mutation, causing increased RNAPII speed, and is suppressed by the rpb2-10 mutation, causing slowed transcription. Thus, Rat1p plays more complex roles in controlling transcription than previously thought.
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影响因子：
16
作者：
Jimeno-Gonzalez, Silvia;Haaning, Line Lindegaard;Jensen, Torben Heick
通讯作者：
Jensen, Torben Heick
影响因子：
10.5
作者：
Luo, WF;Johnson, AW;Bentley, DL
通讯作者：
Bentley, DL
DOI：
10.1073/pnas.90.17.7923
发表时间：
1993-09-01
影响因子：
11.1
作者：
RASMUSSEN, EB;LIS, JT
通讯作者：
LIS, JT
影响因子：
5.3
作者：
Garcia, Alicia;Rosonina, Emanuel;Calvo, Olga
通讯作者：
Calvo, Olga
影响因子：
16
作者：
Ahn, SH;Kim, M;Buratowski, S
通讯作者：
Buratowski, S