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首页> 外文期刊>Cell cycle >CSL protein regulates transcription of genes required to prevent catastrophic mitosis in fission yeast
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CSL protein regulates transcription of genes required to prevent catastrophic mitosis in fission yeast

机译：CSL蛋白调节防止裂变酵母发生灾难性有丝分裂所需的基因的转录

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摘要

For every eukaryotic cell to grow and divide, intricately coordinated action of numerous proteins is required to ensure proper cell-cycle progression. The fission yeast Schizosaccharomyces pombe has been instrumental in elucidating the fundamental principles of cell-cycle control. Mutations in S. pombe 'cut' (cell untimely torn) genes cause failed coordination between cell and nuclear division, resulting in catastrophic mitosis. Deletion of cbf11, a fission yeast CSL transcription factor gene, triggers a 'cut' phenotype, but the precise role of Cbf11 in promoting mitotic fidelity is not known. We report that Cbf11 directly activates the transcription of the acetyl-coenzyme A carboxylase gene cut6, and the biotin uptake/biosynthesis genes vht1 and bio2, with the former 2 implicated in mitotic fidelity. Cbf11 binds to a canonical, metazoan-like CSL response element (GTGGGAA) in the cut6 promoter. Expression of Cbf11 target genes shows apparent oscillations during the cell cycle using temperature-sensitive cdc25-22 and cdc10-M17 block-release experiments, but not with other synchronization methods. The penetrance of catastrophic mitosis in cbf11 and cut6 mutants is nutrient-dependent. We also show that drastic decrease in biotin availability arrests cell proliferation but does not cause mitotic defects. Taken together, our results raise the possibility that CSL proteins play conserved roles in regulating cell-cycle progression, and they could guide experiments into mitotic CSL functions in mammals.
机译：为了使每个真核细胞生长和分裂，需要多种蛋白质的复杂协调作用来确保适当的细胞周期进程。裂殖酵母粟酒裂殖酵母在阐明细胞周期控制的基本原理方面发挥了作用。粟酒裂殖酵母“切割”（细胞不合时宜地撕裂）基因中的突变导致细胞与核分裂之间的协调失败，从而导致灾难性的有丝分裂。裂变酵母CSL转录因子基因cbf11的缺失会触发“切割”表型，但尚不清楚Cbf11在促进有丝分裂保真度中的确切作用。我们报告说Cbf11直接激活乙酰辅酶A羧化酶基因cut6的转录，以及生物素摄取/生物合成基因vht1和bio2，前2个参与有丝分裂保真度。 Cbf11与cut6启动子中的规范，后生动物样CSL反应元件（GTGGGAA）结合。使用温度敏感的cdc25-22和cdc10-M17阻滞释放实验，Cbf11目标基因的表达在细胞周期中显示出明显的振荡，但不使用其他同步方法。 cbf11和cut6突变体中灾难性有丝分裂的外在性取决于养分。我们还表明，生物素利用率的急剧下降会阻止细胞增殖，但不会引起有丝分裂缺陷。综上所述，我们的结果提高了CSL蛋白在调节细胞周期进程中发挥保守作用的可能性，并且它们可以指导哺乳动物中有丝分裂CSL功能的实验。

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