Yeghiayan P, Tu J, Vallier L G, Carlson M
Department of Microbiology, Columbia University, New York, NY 10032, USA.
Yeast. 1995 Mar;11(3):219-24. doi: 10.1002/yea.320110304.
Mutations in the SNF8 gene impair derepression of the SUC2 gene, encoding invertase, in response to glucose limitation of Saccharomyces cerevisiae. We report here the cloning of the SNF8 gene by complementation. Sequence analysis predicts a 26,936-dalton product. Disruption of the chromosomal locus caused a five-fold decrease in invertase derepression, defective growth on raffinose, and a sporulation defect in homozygous diploids. Genetic analysis of the interactions of the snf8 null mutation with spt6/ssn20 and ssn6 suppressors distinguished SNF8 from the groups, SNF1, SNF4 and SNF2, SNF5, SNF6. Notably, the snf8 ssn6 double mutants were extremely sick. Mutations of SNF8 and SNF7 showed similar phenotypes and genetic interactions, and the double mutant combination caused no additional phenotypic impairment. These findings suggest that SNF7 and SNF8 are functionally related.
SNF8基因的突变会损害酿酒酵母在葡萄糖受限的情况下对编码转化酶的SUC2基因的去阻遏作用。我们在此报告通过互补作用克隆SNF8基因。序列分析预测其产物为26,936道尔顿。染色体位点的破坏导致转化酶去阻遏作用降低五倍,在棉子糖上生长缺陷,以及纯合二倍体的孢子形成缺陷。对snf8无效突变与spt6/ssn20和ssn6抑制子相互作用的遗传分析将SNF8与SNF1、SNF4以及SNF2、SNF5、SNF6区分开来。值得注意的是,snf8 ssn6双突变体极其虚弱。SNF8和SNF7的突变表现出相似的表型和遗传相互作用,并且双突变组合并未导致额外的表型损伤。这些发现表明SNF7和SNF8在功能上相关。