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抑制酵母中上游激活序列缺失的突变:一种蛋白激酶和组蛋白H3在体内抑制转录中的作用

Mutations that suppress the deletion of an upstream activating sequence in yeast: involvement of a protein kinase and histone H3 in repressing transcription in vivo.

作者信息

Prelich G, Winston F

机构信息

Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115.

出版信息

Genetics. 1993 Nov;135(3):665-76. doi: 10.1093/genetics/135.3.665.

Abstract

Regulated transcription of most protein-encoding genes in Saccharomyces cerevisiae requires an upstream activating sequence (UAS); in the absence of UAS elements, little or no transcription occurs. In certain mutant strains, however, promoters that have been deleted for their UAS can direct significant levels of transcription, indicating that the remaining promoter elements (the basal promoter) are capable of directing higher levels of transcription, but they are normally represented in wild-type strains. To analyze this repression, we have selected for mutations that cause increased transcription of the SUC2 gene in the absence of its UAS. In addition to some previously studied genes, this selection has identified five genes that we have designated BUR1, BUR2, BUR3, BUR5 and BUR6 (for Bypass UAS Requirement). The bur mutations cause pleiotropic phenotypes, indicating that they affect transcription of many genes. Furthermore, some bur mutations suppress the requirement for the SNF5 trans-activator at both SUC2 and Ty. Additional analysis has demonstrated that BUR1 is identical to SGV1, which encodes a CDC28-related protein kinase. This result indicates that protein phosphorylation is important for repression of the SUC2 basal promoter as well as other aspects of transcription in vivo. Finally, BUR5 is identical to HHT1, encoding histone H3, further implicating chromatin structure as important for expression of SUC2.

摘要

酿酒酵母中大多数蛋白质编码基因的转录调控需要上游激活序列(UAS);在没有UAS元件的情况下,转录很少或根本不发生。然而,在某些突变菌株中,其UAS已被删除的启动子可以指导显著水平的转录,这表明剩余的启动子元件(基础启动子)能够指导更高水平的转录,但它们在野生型菌株中通常受到抑制。为了分析这种抑制作用,我们选择了在没有SUC2基因的UAS时能导致其转录增加的突变。除了一些先前研究过的基因外,这种选择还鉴定出了五个基因,我们将其命名为BUR1、BUR2、BUR3、BUR5和BUR6(用于绕过UAS需求)。bur突变会导致多效性表型,表明它们影响许多基因的转录。此外,一些bur突变抑制了SUC2和Ty处对SNF5反式激活因子的需求。进一步的分析表明,BUR1与SGV1相同,后者编码一种与CDC28相关的蛋白激酶。这一结果表明,蛋白质磷酸化对于体内SUC2基础启动子的抑制以及转录的其他方面都很重要。最后,BUR5与HHT1相同,后者编码组蛋白H3,这进一步表明染色质结构对于SUC2的表达很重要。

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