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首页> 外文期刊>Cell cycle >Coupling of RNA polymerase III assembly to cell cycle progression in Saccharomyces cerevisiae
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Coupling of RNA polymerase III assembly to cell cycle progression in Saccharomyces cerevisiae

机译：RNA聚合酶III组装在酿酒酵母中细胞周期进展的偶联

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摘要

Assembly of the RNA polymerases in both yeast and humans is proposed to occur in the cytoplasm prior to their nuclear import. Our previous studies identified a cold-sensitive mutation, rpc128-1007, in the yeast gene encoding the second largest Pol III subunit, Rpc128. rpc128-1007 is associated with defective assembly of Pol III complex and, in consequence, decreased level of tRNA synthesis. Here, we show that rpc128-1007 mutant cells remain largely unbudded and larger than wild type cells. Flow cytometry revealed that most rpc128-1007 mutant cells have G1 DNA content, suggesting that this mutation causes pronounced cell cycle delay in the G1 phase. Increased expression of gene encoding Rbs1, the Pol III assembly/import factor, could counteract G1 arrest observed in the rpc128-1007 mutant and restore wild type morphology of mutant cells. Concomitantly, cells lacking Rbs1 show a mild delay in G1 phase exit, indicating that Rbs1 is required for timely cell cycle progression. Using the double rpc128-1007 maf1 Delta mutant in which tRNA synthesis is recovered, we confirmed that the Pol III assembly defect associated with rpc128-1007 is a primary cause of cell cycle arrest. Together our results indicate that impairment of Pol III complex assembly is coupled to cell cycle inhibition in the G1 phase.
机译：提出在核癌前的细胞质中组装酵母和人类中的RNA聚合酶。我们以前的研究发现了在编码第二大POL III亚基RPC128的酵母基因中，鉴定了一种冷敏感性突变RPC128-1007。 RPC128-1007与POL III复合物的缺陷组装有关，结果降低了TRNA合成水平。在这里，我们表明RPC128-1007突变细胞仍然很大程度上不一于且大于野生型细胞。流式细胞术显示大多数RPC128-1007突变体细胞具有G1 DNA含量，表明该突变导致G1相中发明细胞周期延迟。增加了编码RBS1，POL III组装/导入因子的基因表达，可以抵消RPC128-1007突变体和恢复突变细胞的野生型形态中观察到的G1骤停。伴随地，缺乏RBS1的细胞显示出G1相出的温和延迟，表明RBS1是用于及时细胞周期进展所必需的。使用TRNA合成被回收的双RPC128-1007 MAF1衍射突变体，我们证实了与RPC128-1007相关的POL III组装缺陷是细胞周期停滞的主要原因。我们的结果表明，POL III复杂组件的损害与G1相中的细胞周期抑制偶联。

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