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首页> 外文期刊>Molecular and Cellular Biology >Replication Fork Progression Is Impaired by Transcription in Hyperrecombinant Yeast Cells Lacking a Functional THO Complex
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Replication Fork Progression Is Impaired by Transcription in Hyperrecombinant Yeast Cells Lacking a Functional THO Complex

机译：复制叉进展受到缺乏功能性THO复杂的超重组酵母细胞中的转录的影响。

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THO/TREX is a conserved, eukaryotic protein complex operating at the interface between transcription and messenger ribonucleoprotein (mRNP) metabolism. THO mutations impair transcription and lead to increased transcription-associated recombination (TAR). These phenotypes are dependent on the nascent mRNA; however, the molecular mechanism by which impaired mRNP biogenesis triggers recombination in THO/TREX mutants is unknown. In this study, we provide evidence that deficient mRNP biogenesis causes slowdown or pausing of the replication fork in hpr1Δ mutants. Impaired replication appears to depend on sequence-specific features since it was observed upon activation of lacZ but not leu2 transcription. Replication fork progression could be partially restored by hammerhead ribozyme-guided self-cleavage of the nascent mRNA. Additionally, hpr1Δ increased the number of S-phase but not G2-dependent TAR events as well as the number of budded cells containing Rad52 repair foci. Our results link transcription-dependent genomic instability in THO mutants with impaired replication fork progression, suggesting a molecular basis for a connection between inefficient mRNP biogenesis and genetic instability.
机译：THO / TREX是一种保守的真核蛋白质复合体，在转录和信使核糖核蛋白（mRNP）代谢之间的界面运行。 THO突变损害转录并导致转录相关重组（TAR）增加。这些表型取决于新生的mRNA。然而，受损的mRNP生物发生触发THO / TREX突变体重组的分子机制尚不清楚。在这项研究中，我们提供证据，证明mRNP的生物发生不足会导致hpr1Δ突变体的复制叉减慢或暂停。复制受损似乎取决于序列特异性特征，因为在激活 lacZ 但未激活 leu2 时观察到。锤头状核酶引导的新生mRNA自我切割可部分恢复复制叉的进展。此外，hpr1Δ增加了S期而不依赖G 2 的TAR事件的数量，并且增加了包含Rad52修复灶的芽细胞的数量。我们的结果将THO突变体中转录依赖的基因组不稳定性与复制叉的进展受损联系起来，这表明低效mRNP生物发生与遗传不稳定性之间存在联系的分子基础。

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