酿酒酵母GAL1启动子的URSG介导的葡萄糖阻遏分析。
Analysis of URSG-mediated glucose repression of the GAL1 promoter of Saccharomyces cerevisiae.
作者信息
Flick J S, Johnston M
机构信息
Department of Genetics, Washington University Medical School, St. Louis, Missouri 63110.
出版信息
Genetics. 1992 Feb;130(2):295-304. doi: 10.1093/genetics/130.2.295.
Abstract
Repression of GAL1 expression during growth on glucose is mediated in part by cis-acting promoter elements designated URSG. We show that oligonucleotides containing sequences from two regions of URSG confer glucose repression upon a heterologous promoter. Repression caused by URSG is dependent on trans-acting factors of the glucose repression pathway and is independent of orientation or location within a promoter, suggesting that URSG contains binding sites for a glucose-activated repressor protein(s). Genetic analysis identified three apparently novel genes (URR1, URR3 and URR4) that are specifically required for URSG-mediated repression and may encode such repressor proteins. Mutations in the URR genes suppress the defect in URSG derepression caused by a snf1 mutation.
摘要
在葡萄糖上生长期间，GAL1表达的抑制部分是由称为URSG的顺式作用启动子元件介导的。我们表明，含有来自URSG两个区域序列的寡核苷酸赋予异源启动子葡萄糖抑制作用。URSG引起的抑制依赖于葡萄糖抑制途径的反式作用因子，并且与启动子内的方向或位置无关，这表明URSG含有葡萄糖激活的阻遏蛋白的结合位点。遗传分析鉴定出三个明显的新基因（URR1、URR3和URR4），它们是URSG介导的抑制所特需的，并且可能编码这种阻遏蛋白。URR基因中的突变抑制了由snf1突变引起的URSG去抑制缺陷。
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本文引用的文献
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