Neigeborn L, Carlson M
Genetics. 1984 Dec;108(4):845-58. doi: 10.1093/genetics/108.4.845.
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.
分离出了在蔗糖或棉子糖发酵方面存在缺陷的酿酒酵母突变体。除了蔗糖酶结构基因SUC2中的突变外,我们还获得了18个隐性突变,这些突变影响了葡萄糖阻遏对蔗糖酶合成的调控。这些突变包括5个新的snf1(蔗糖不发酵)等位基因,还定义了5个新的互补群,分别命名为snf2、snf3、snf4、snf5和snf6。snf2、snf4和snf5突变体在去阻遏条件下产生很少或不产生分泌型蔗糖酶,并且在半乳糖和甘油利用方面存在多效性缺陷,而这两者均受葡萄糖阻遏调控。snf6突变体在去阻遏条件下产生低水平的分泌型蔗糖酶,未检测到多效性。snf3突变体将分泌型蔗糖酶去阻遏至野生型水平的10% - 35%,但在蔗糖上生长不如根据其蔗糖酶活性预期的那样好;此外,snf3突变体在葡萄糖阻遏条件下合成了一些蔗糖酶。我们研究了不同的snf突变与ssn6之间的相互作用,ssn6是一种导致组成型(葡萄糖不敏感)高水平蔗糖酶合成的突变,先前作为snf1的抑制子被分离出来。ssn6突变完全抑制了由snf1、snf3、snf4和snf6赋予的蔗糖酶去阻遏缺陷,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型。相比之下,snf2 ssn6和snf5 ssn6菌株在去阻遏条件下仅产生中等水平 的蔗糖酶,在阻遏条件下产生极低水平的蔗糖酶。这些发现表明SNF1至SNF6和SSN6基因在通过葡萄糖阻遏调控SUC2基因表达中发挥作用。