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首页> 外文期刊>Molecular and Cellular Biology >Cell cycle arrest caused by CLN gene deficiency in Saccharomyces cerevisiae resembles START-I arrest and is independent of the mating-pheromone signalling pathway.
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Cell cycle arrest caused by CLN gene deficiency in Saccharomyces cerevisiae resembles START-I arrest and is independent of the mating-pheromone signalling pathway.

机译：由酿酒酵母中的CLN基因缺陷引起的细胞周期停滞类似于START-I停滞，并且独立于交配信息素信号通路。

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摘要

Null mutations in three genes encoding cyclin-like proteins (CLN1, CLN2, and CLN3) in Saccharomyces cerevisiae cause cell cycle arrest in G1 (cln arrest). In cln1 cln2 cln3 strains bearing plasmids containing the CLN3 (also called WHI1 or DAF1) coding sequence under the transcriptional control of a galactose-regulated promoter, shift from galactose to glucose medium (shutting off synthesis of CLN3 mRNA) allowed completion of cell cycles in progress but caused arrest in the ensuing unbudded G1 phase. Cell growth was not inhibited in arrested cells. Cell division occurred in glucose medium even if cells were arrested in S phase during the initial 2 h of glucose treatment, suggesting that CLN function may not be required in the cell cycle after S phase. However, when the coding sequence of the hyperactive C-terminal truncation allele CLN3-2 (formerly DAF1-1) was placed under GAL control, cells went through multiple cycles before arresting after a shift from galactose to glucose. These results suggest that the C terminus of the wild-type protein confers functional instability. cln-arrested cells are mating competent. However, cln arrest is distinct from constitutive activation of the mating-factor signalling pathway because cln-arrested cells were dependent on the addition of pheromone both for mating and for induction of an alpha-factor-induced transcript, FUS1, and because MATa/MAT alpha (pheromone-nonresponsive) strains were capable of cln arrest in G1 (although a residual capacity for cell division before arrest was observed in MATa/MAT alpha strains). These results are consistent with a specific CLN requirement for START transit.
机译：酿酒酵母中编码细胞周期蛋白样蛋白（CLN1，CLN2和CLN3）的三个基因的空突变导致细胞周期停滞在G1中（cln停滞）。在带有含CLN3（也称为WHI1或DAF1）编码序列的质粒的cln1 cln2 cln3菌株中，其在半乳糖调节的启动子的转录控制下，从半乳糖转移至葡萄糖培养基（切断CLN3 mRNA的合成），从而完成了细胞周期的调控。进步，但在随后的未预算的G1阶段遭到逮捕。在停滞的细胞中细胞生长不受抑制。即使在葡萄糖处理的最初2小时内将细胞停滞在S期中，葡萄糖培养基中也会发生细胞分裂，这表明在S期后的细胞周期中可能不需要CLN功能。但是，当将高活性C端截短等位基因CLN3-2（以前称为DAF1-1）的编码序列置于GAL的控制下时，细胞经历了多个循环，然后从半乳糖变为葡萄糖后停滞。这些结果表明野生型蛋白的C末端赋予功能不稳定。 cln阻滞细胞交配能力。但是，cln阻滞不同于交配因子信号通路的组成性激活，因为cln被阻滞的细胞在交配和诱导α因子诱导的转录本FUS1时都依赖信息素的添加，并且因为MATa / MAT α（信息素无反应）菌株能够在G1中进行cln阻滞（尽管在MATa / MATα菌株中观察到了阻滞前的细胞分裂残留能力）。这些结果与START转运的特定CLN要求一致。

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