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CLN3而非正反馈决定了循环细胞中CLN2转录的时间。

CLN3, not positive feedback, determines the timing of CLN2 transcription in cycling cells.

作者信息

Stuart D, Wittenberg C

机构信息

Department of Molecular Biology, Scripps Research Institute, La Jolla, California 92037, USA.

出版信息

Genes Dev. 1995 Nov 15;9(22):2780-94. doi: 10.1101/gad.9.22.2780.

Abstract

Transcriptional activation of the budding yeast CLN1 and CLN2 genes during the late G1 phase of the cell cycle has been attributed to a positive feedback loop, wherein the transcription of both genes is stimulated by the accumulation of their protein products. We demonstrate that in cycling cells CLN2 does not play a role in determining the timing of its own transcriptional activation. First, we show that CLN3 alone is sufficient to maximally activate CLN2 transcription. Cells that lack functional CLN1 and CLN2 genes activate the CLN2 promoter with the same kinetics and at the same size as cells in which all three CLN genes are functional. In addition, CLN2 transcription is activated with similar kinetics in cells that have CLN2 as their only functional CLN gene and in CLN-deficient cells. Promoter analysis shows that CLN3-dependent activation of CLN2 transcription is directed primarily through the previously identified UAS1 region although another cis-acting region, UAS2, also can contribute to CLN2 activation under some conditions. The ability to activate transcription of CLN2 is not a unique property of CLN3 because ectopically expressed CLN2 can both activate the endogenous CLN2 promoter and induce Start. We propose that failure of the endogenous CLN2 gene to contribute significantly to activation of its own transcription results from its relative effectiveness at inducing Start, cell cycle progression and, subsequently, inactivation of CLN2 expression.

摘要

在细胞周期的G1期后期,芽殖酵母CLN1和CLN2基因的转录激活归因于一个正反馈环,其中这两个基因的转录受到其蛋白质产物积累的刺激。我们证明,在循环细胞中,CLN2在决定其自身转录激活的时间方面不起作用。首先,我们表明单独的CLN3足以最大程度地激活CLN2转录。缺乏功能性CLN1和CLN2基因的细胞激活CLN2启动子的动力学和细胞大小与所有三个CLN基因均具有功能的细胞相同。此外,在以CLN2作为唯一功能性CLN基因的细胞和CLN缺陷型细胞中,CLN2转录以相似的动力学被激活。启动子分析表明,CLN3依赖的CLN2转录激活主要通过先前鉴定的UAS1区域介导,尽管另一个顺式作用区域UAS2在某些条件下也可促进CLN2的激活。激活CLN2转录的能力不是CLN3的独特特性,因为异位表达的CLN2既可以激活内源性CLN2启动子,也可以诱导起始点。我们提出,内源性CLN2基因未能对其自身转录激活做出重大贡献,是由于其在诱导起始点、细胞周期进程以及随后使CLN2表达失活方面的相对有效性。

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