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增加MSN1基因的剂量可恢复在SNF1蛋白激酶缺陷的酵母突变体中的转化酶表达。

Increased dosage of the MSN1 gene restores invertase expression in yeast mutants defective in the SNF1 protein kinase.

作者信息

Estruch F, Carlson M

机构信息

Department of Genetics, Columbia University College of Physicians and Surgeons, New York, 10032.

出版信息

Nucleic Acids Res. 1990 Dec 11;18(23):6959-64. doi: 10.1093/nar/18.23.6959.

Abstract

The SNF1 protein kinase is required for expression of the invertase gene in response to glucose deprivation in Saccharomyces cerevisiae. We selected for genes that in multicopy suppress the invertase defect of temperature-sensitive snf1 mutants. Increased dosage of the MSN1 gene restores high-level, regulated invertase expression in snf1-ts mutants, and disruption of MSN1 in the wild type reduces invertase expression a fewfold. MSN1 gene dosage does not affect SNF1 protein kinase activity in vitro. MSN1 encodes a 43-kilodalton protein, and a MSN1-beta-galactosidase fusion protein was localized in the nucleus. A LexA-MSN1 fusion protein, when bound to a lexA operator, activates transcription of an adjacent promoter. In vitro synthesized MSN1 protein exhibits weak, nonspecific DNA-binding activity.

摘要

在酿酒酵母中,SNF1蛋白激酶是响应葡萄糖剥夺时蔗糖酶基因表达所必需的。我们筛选了多拷贝状态下能抑制温度敏感型snf1突变体蔗糖酶缺陷的基因。MSN1基因剂量增加可恢复snf1-ts突变体中高水平、受调控的蔗糖酶表达,而野生型中MSN1的缺失会使蔗糖酶表达降低几倍。MSN1基因剂量在体外不影响SNF1蛋白激酶活性。MSN1编码一种43千道尔顿的蛋白质,并且MSN1-β-半乳糖苷酶融合蛋白定位于细胞核中。当LexA-MSN1融合蛋白与lexA操纵基因结合时,可激活相邻启动子的转录。体外合成的MSN1蛋白表现出微弱的非特异性DNA结合活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c62f/332756/27262b2a57bf/nar00207-0212-a.jpg

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