Genes affecting the regulation of SUC2 gene expression by glucose repression in Saccharomyces cerevisiae.
Genes affecting the regulation of SUC2 gene expression by glucose repression in Saccharomyces cerevisiae.
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DOI：
10.1093/genetics/108.4.845
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发表时间：
1984-12
期刊：
影响因子：
3.3
通讯作者：
L. Neigeborn;M. Carlson
中科院分区：
文献类型：
--
作者：
L. Neigeborn;M. Carlson
分离出蔗糖或棉子糖发酵缺陷的酿酒酵母突变体。除了蔗糖酶的 SUC2 结构基因突变外，我们还发现了 18 个隐性突变，这些突变通过葡萄糖抑制影响蔗糖酶合成的调节。这些突变包括五个新的 snf1（蔗糖非发酵）等位基因，还定义了五个新的互补组，称为 snf2、snf3、snf4、snf5 和 snf6。 snf2、snf4 和 snf5 突变体在去抑制条件下几乎不产生或不产生分泌性转化酶，并且在半乳糖和甘油利用方面存在多效性缺陷，而半乳糖和甘油利用均受到葡萄糖抑制的调节。 snf6突变体在去抑制条件下产生低水平的分泌型转化酶，并且没有检测到多效性。 snf3突变体将分泌的蔗糖酶去抑制至野生型水平的10-35%，但在蔗糖上的生长不如其蔗糖酶活性预期的那样好；此外，snf3 突变体在葡萄糖抑制条件下合成了一些转化酶。--我们检查了不同 snf 突变和 ssn6 之间的相互作用，ssn6 是一种导致组成型（葡萄糖不敏感）高水平转化酶合成的突变，之前被分离为 snf1 的抑制剂。 ssn6突变完全抑制了snf1、snf3、snf4和snf6所赋予的蔗糖酶去抑制缺陷，并且每个双突变体都表现出ssn6单突变体典型的蔗糖酶组成性。相比之下，snf2 ssn6 和 snf5 ssn6 菌株在去抑制条件下仅产生中等水平的蔗糖酶，而在抑制条件下产生非常低的水平。这些发现表明 SNF1 至 SNF6 和 SSN6 基因在通过葡萄糖抑制调节 SUC2 基因表达中的作用。
Mutants of Saccharomyces cerevisiae with defects in sucrose or raffinose fermentation were isolated. In addition to mutations in the SUC2 structural gene for invertase, we recovered 18 recessive mutations that affected the regulation of invertase synthesis by glucose repression. These mutations included five new snf1 (sucrose nonfermenting) alleles and also defined five new complementation groups, designated snf2, snf3, snf4, snf5, and snf6. The snf2, snf4, and snf5 mutants produced little or no secreted invertase under derepressing conditions and were pleiotropically defective in galactose and glycerol utilization, which are both regulated by glucose repression. The snf6 mutant produced low levels of secreted invertase under derepressing conditions, and no pleiotropy was detected. The snf3 mutants derepressed secreted invertase to 10-35% the wild-type level but grew less well on sucrose than expected from their invertase activity; in addition, snf3 mutants synthesized some invertase under glucose-repressing conditions.--We examined the interactions between the different snf mutations and ssn6, a mutation causing constitutive (glucose-insensitive) high-level invertase synthesis that was previously isolated as a suppressor of snf1. The ssn6 mutation completely suppressed the defects in derepression of invertase conferred by snf1, snf3, snf4 and snf6, and each double mutant showed the constitutivity for invertase typical of ssn6 single mutants. In contrast, snf2 ssn6 and snf5 ssn6 strains produced only moderate levels of invertase under derepressing conditions and very low levels under repressing conditions. These findings suggest roles for the SNF1 through SNF6 and SSN6 genes in the regulation of SUC2 gene expression by glucose repression.