A suppressor of SNF1 mutations causes constitutive high-level invertase synthesis in yeast.

A suppressor of SNF1 mutations causes constitutive high-level invertase synthesis in yeast.
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DOI:
10.1093/genetics/107.1.19
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发表时间:
1984-05
期刊:
影响因子:
3.3
通讯作者:
M. Carlson;B. Osmond;L. Neigeborn;D. Botstein
M. Carlson;B. Osmond;L. Neigeborn;D. Botstein
中科院分区:
生物学2区
文献类型:
--
作者:
M. Carlson;B. Osmond;L. Neigeborn;D. Botstein

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酿酒酵母的SNF 1基因产物需要去抑制许多葡萄糖抑制基因的表达,包括转化酶的SUC 2结构基因。携带隐性snf 1突变的菌株不能发酵蔗糖。我们已经分离出30个snf 1突变体的部分表型回复突变体,能够发酵蔗糖。这些回复突变体的遗传特性表明,抑制突变都是隐性的,并定义了8个互补组,指定ssn 1到ssn 8(抑制snf 1)。测定了回复突变体的分泌转化酶活性,虽然在每个互补组的成员中检测到活性,但只有ssn 6菌株含有野生型水平。ssn 6菌株分泌型转化酶的合成被认为是组成型的,即对葡萄糖抑制不敏感;此外,ssn 6突变还赋予野生型(SNF 1)遗传背景中的组成性,因此,不仅仅是SNF 1的抑制因子。在ssn 6突变体中观察到多效性缺陷。遗传分析表明ssn 6突变与R.罗斯坦和F.谢尔曼,导致异2-细胞色素c的产生增加。这些数据表明SSN 6的调节功能。
The SNF1 gene product of Saccharomyces cerevisiae is required to derepress expression of many glucose-repressible genes, including the SUC2 structural gene for invertase. Strains carrying a recessive snf1 mutation are unable to ferment sucrose. We have isolated 30 partial phenotypic revertants of a snf1 mutant that were able to ferment sucrose. Genetic characterization of these revertants showed that the suppressor mutations were all recessive and defined eight complementation groups, designated ssn1 through ssn8 (suppressor of snf1 ). The revertants were assayed for secreted invertase activity, and although activity was detected in members of each complementation group, only the ssn6 strains contained wild-type levels. Synthesis of secreted invertase in ssn6 strains was found to be constitutive, that is, insensitive to glucose repression; moreover, the ssn6 mutations also conferred constitutivity in a wild-type ( SNF1 ) genetic background and are, therefore, not merely suppressors of snf1 . Pleiotropic defects were observed in ssn6 mutants. Genetic analysis suggested that the ssn6 mutations are allelic to the cyc8 mutation isolated by R. J. Rothstein and F. Sherman, which causes increased production of iso-2-cytochrome c. The data suggest a regulatory function for SSN6 .