The essential helicase-like protein Sen1 mediates termination of RNA Polymerase II (Pol II) transcription at snoRNAs and other noncoding RNAs in yeast. A mutation in the Pol II subunit Rpb1 that increases the elongation rate increases read-through transcription at Sen1-mediated terminators. Termination and growth defects in sen1 mutant cells are partially suppressed by a slowly transcribing Pol II mutant and are exacerbated by a faster-transcribing Pol II mutant. Deletion of the nuclear exosome subunit Rrp6 allows visualization of noncoding RNA intermediates that are terminated but not yet processed. Sen1 mutants or faster-transcribing Pol II increase the average lengths of preprocessed snoRNA, CUT, and SUT transcripts, while slowed Pol II transcription produces shorter transcripts. These connections between transcription rate and Sen1 activity support a model whereby kinetic competition between elongating Pol II and Sen1 helicase establishes the temporal and spatial window for early Pol II termination.

译文

必需的解旋酶样蛋白Sen1介导RNA聚合酶II (Pol II) 在酵母中的snoRNAs和其他非编码RNA上的转录终止。增加伸长率的Pol II亚基Rpb1中的突变增加了Sen1-mediated终止子处的通读转录。缓慢转录的Pol II突变体部分抑制了sen1突变细胞中的终止和生长缺陷,而转录速度较快的Pol II突变体则加剧了这种缺陷。删除核外泌体亚基Rrp6允许可视化终止但尚未处理的非编码RNA中间体。Sen1突变体或转录速度较快的Pol II增加了预处理的snoRNA,CUT和SUT转录物的平均长度,而减慢Pol II转录速度会产生较短的转录物。转录速率与Sen1活性之间的这些联系支持了一个模型,该模型使延长的Pol II和Sen1解旋酶之间的动力学竞争建立了早期Pol II终止的时间和空间窗口。

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