Genetic and molecular characterization of GAL83: its interaction and similarities with other genes involved in glucose repression in Saccharomyces cerevisiae.
Genetic and molecular characterization of GAL83: its interaction and similarities with other genes involved in glucose repression in Saccharomyces cerevisiae.
复制标题
GAL83 的遗传和分子特征：其与酿酒酵母中参与葡萄糖抑制的其他基因的相互作用和相似性。
DOI：
10.1093/genetics/135.3.655
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发表时间：
1993
期刊：
影响因子：
3.3
通讯作者：
Johnston,M
中科院分区：
文献类型：
--
作者：
Erickson,JR;Johnston,M
酿酒酵母 GAL 基因的表达受到葡萄糖抑制，这是一种需要多种基因产物的全局调节机制。我们分离出了 GAL83，这是葡萄糖抑制所需的基因之一。预测的 Gal83 蛋白的序列与其他两种酵母蛋白 Sip1p 和 Sip2p 同源，已知它们与 SNF1 基因产物（一种 GAL 基因表达所需的蛋白激酶）相互作用。 SIP1 和 SIP2 的高拷贝克隆交叉互补 GAL83-2000 突变（以及 GAL82-1，另一个参与葡萄糖抑制的基因的突变），表明这四个基因可能在葡萄糖抑制中发挥相似的功能。与这一假设一致，gal83 无效突变不会影响葡萄糖抑制，并且 GAL83（和 GAL82）中仅存在显性或部分显性突变。另外两个观察结果表明，GAL83 与 GAL82 和 REG1（另一种参与葡萄糖抑制的基因）相互依赖地发挥作用，从而影响葡萄糖抑制：1) 低拷贝质粒上的 REG1 交叉互补 GAL82-1 和 GAL83-2000 突变，2) reg1、GAL82-1 和 GAL83-2000 的所有成对组合都无法相互互补。这种不相关的非互补性表明 Gal83p、Gal82p 和 Reg1p 可能彼此相互作用。 GAL83、GAL82 和 REG1 的可能作用将结合 SNF1、SIP1 和 SIP2 进行讨论。
Expression of the GAL genes of Saccharomyces cerevisiae is subject to glucose repression, a global regulatory mechanism that requires several gene products. We have isolated GAL83, one of these genes required for glucose repression. The sequence of the predicted Gal83 protein is homologous to two other yeast proteins, Sip1p and Sip2p, which are known to interact with the SNF1 gene product, a protein kinase required for expression of the GAL genes. High-copy clones of SIP1 and SIP2 cross-complement the GAL83-2000 mutation (as well as GAL82-1, a mutation in another gene involved in glucose repression), suggesting that these four genes may perform similar functions in glucose repression. Consistent with this hypothesis, a gal83 null mutation does not affect glucose repression, and only dominant or partially dominant mutations exist in GAL83 (and GAL82). Two other observations were made that suggests that GAL83 functions interdependently with GAL82 and REG1 (another gene involved in glucose repression) to effect glucose repression: 1) REG1 on a low-copy plasmid cross-complements GAL82-1 and GAL83-2000 mutations, and 2) all pairwise combinations of reg1, GAL82-1 and GAL83-2000 fail to complement one another. Such unlinked noncomplementation suggests that Gal83p, Gal82p and Reg1p may interact with one another. Possible roles for GAL83, GAL82 and REG1 are discussed in relation to SNF1, SIP1 and SIP2.