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酿酒酵母己糖激酶2基因启动子区域的分子分析。

Molecular analysis of the promoter region of the hexokinase 2 gene of Saccharomyces cerevisiae.

作者信息

Martínez-Campa C, Herrero P, Ramírez M, Moreno F

机构信息

Departamento de Bioquímica y Biología Molecular, Universidad de Oviedo, Spain.

出版信息

FEMS Microbiol Lett. 1996 Mar 15;137(1):69-74. doi: 10.1111/j.1574-6968.1996.tb08084.x.

DOI:10.1111/j.1574-6968.1996.tb08084.x
PMID:8935659
Abstract

lacZ fusions of the hexokinase 2 gene promoter were constructed and a deletion analysis was performed in order to identify the cis-acting regulatory elements of the promoter that controls hexokinase 2 gene expression. Expression of the hexokinase 2 gene is induced by glucose and around 40-fold repressed by ethanol. This repression seems to be mediated mainly by a repression element located within the coding region of the hexokinase 2 gene, between +39 and +404 bp from the ATG start codon. A second repressing element for ethanol growing cells was located between -455 bp and -254 bp. A synergistic effect on repression of transcription, when ethanol is the carbon source used for growth, was demonstrated by experiments in which both repressing elements were simultaneously removed. The finding of regulatory sequences in the coding region of the hexokinase 2 gene stimulates a search for regulatory elements in the coding region of other yeast genes.

摘要

构建了己糖激酶2基因启动子的lacZ融合体,并进行了缺失分析,以鉴定控制己糖激酶2基因表达的启动子顺式作用调控元件。己糖激酶2基因的表达受葡萄糖诱导,而受乙醇抑制约40倍。这种抑制似乎主要由位于己糖激酶2基因编码区内、距ATG起始密码子+39至+404 bp之间的一个抑制元件介导。乙醇生长细胞的第二个抑制元件位于-455 bp和-254 bp之间。通过同时去除两个抑制元件的实验证明,当乙醇作为生长所用碳源时,对转录抑制具有协同作用。在己糖激酶2基因编码区发现调控序列,促使人们在其他酵母基因的编码区寻找调控元件。

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引用本文的文献

1
The hexokinase 2 protein regulates the expression of the GLK1, HXK1 and HXK2 genes of Saccharomyces cerevisiae.己糖激酶2蛋白调节酿酒酵母的GLK1、HXK1和HXK2基因的表达。
Biochem J. 2001 May 1;355(Pt 3):625-31. doi: 10.1042/bj3550625.
2
Carbon source-dependent phosphorylation of hexokinase PII and its role in the glucose-signaling response in yeast.己糖激酶PII的碳源依赖性磷酸化及其在酵母葡萄糖信号应答中的作用。
Mol Cell Biol. 1998 May;18(5):2940-8. doi: 10.1128/MCB.18.5.2940.