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Genes Affecting the Regulation of SUC2 Gene Expression by Glucose Repression in SACCHAROMYCES CEREVISIAE

机译:酿酒酵母中葡萄糖阻抑作用影响SUC2基因表达调控的基因

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摘要

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.
机译:分离出具有蔗糖或棉子糖发酵缺陷的酿酒酵母突变体。除了用于转化酶的SUC2结构基因中的突变外,我们还回收了18个隐性突变,这些突变影响了葡萄糖抑制对转化酶合成的调节。这些突变包括五个新的snf1(蔗糖非发酵)等位基因,并且还定义了五个新的互补组,称为snf2,snf3,snf4,snf5和snf6。 snf2,snf4和snf5突变体在减压条件下几乎不分泌分泌的转化酶,并且在半乳糖和甘油利用方面均存在多效性缺陷,这两个途径均受葡萄糖抑制的调节。 snf6突变体在减压条件下产生低水平的分泌型转化酶,并且未检测到多效性。 snf3突变体抑制了分泌的转化酶至野生型水平的10-35%,但在蔗糖上的生长却比其转化酶活性预期的要差。此外,snf3突变体在抑制葡萄糖的条件下合成了一些转化酶。-我们研究了不同的snf突变与ssn6之间的相互作用,该突变导致组成型(对葡萄糖不敏感的)高水平转化酶的合成,该突变以前被分离为snf1的抑制剂。 。 ssn6突变完全抑制了snf1,snf3,snf4和snf6赋予的转化酶抑制抑制的缺陷,每个双突变体均表现出 ssn6 单突变体典型的转化酶组成性。相反, snf2 ssn6 snf5 ssn6 菌株在降压条件下仅产生中等水平的转化酶,而在抑制条件下仅产生低水平的转化酶。这些发现表明 SNF1 SNF6 SSN6 基因在葡萄糖抑制调控 SUC2 基因表达中的作用。

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