Neigeborn L, Schwartzberg P, Reid R, Carlson M
Mol Cell Biol. 1986 Nov;6(11):3569-74. doi: 10.1128/mcb.6.11.3569-3574.1986.
Missense mutations in the SNF3 gene of Saccharomyces cerevisiae were previously found to cause defects in both glucose repression and derepression of the SUC2 (invertase) gene. In addition, the growth properties of snf3 mutants suggested that they were defective in uptake of glucose and fructose. We have cloned the SNF3 gene by complementation and demonstrated linkage of the cloned DNA to the chromosomal SNF3 locus. The gene encodes a 3-kilobase poly(A)-containing RNA, which was fivefold more abundant in cells deprived of glucose. The SNF3 gene was disrupted at its chromosomal locus by several methods to create null mutations. Disruption resulted in growth phenotypes consistent with a defect in glucose uptake. Surprisingly, gene disruption did not cause aberrant regulation of SUC2 expression. We discuss possible mechanisms by which abnormal SNF3 gene products encoded by missense alleles could perturb regulatory functions.
先前发现，酿酒酵母SNF3基因中的错义突变会导致SUC2（转化酶）基因的葡萄糖阻遏和去阻遏缺陷。此外，snf3突变体的生长特性表明它们在葡萄糖和果糖摄取方面存在缺陷。我们通过互补作用克隆了SNF3基因，并证明克隆的DNA与染色体SNF3位点存在连锁关系。该基因编码一种含有3千碱基聚腺苷酸的RNA，在缺乏葡萄糖的细胞中其丰度要高五倍。通过几种方法在其染色体位点破坏SNF3基因以产生无效突变。破坏导致的生长表型与葡萄糖摄取缺陷一致。令人惊讶的是，基因破坏并未导致SUC2表达的异常调控。我们讨论了错义等位基因编码的异常SNF3基因产物可能干扰调控功能的机制。
