Vagnoli P, Bisson L F
Department of Viticulture and Enology, University of California at Davis 95616-8749, USA.
Yeast. 1998 Mar 15;14(4):359-69. doi: 10.1002/(SICI)1097-0061(19980315)14:4<359::AID-YEA227>3.0.CO;2-#.
The SKS1 gene was originally identified as a multicopy suppressor of the growth defect of snf3 null mutations on low glucose concentrations. Snf3p is required for the rapid induction of HXT2 during growth on low substrate concentrations. Loss of Snf3p leads to a dramatic delay in expression of HXT2. Adaptation to low substrate concentrations does not occur in snf3 sks1 double null mutant strains, suggesting that SKS1 is required for the glucose-dependent expression of HXT2 in the absence of Snf3p activity. Over-expression of SKS1 leads to over-expression of Hxt2p, thus explaining the mechanism of suppression of the snf3 defect. SKS1 defines a novel, Snf3p-independent pathway for the expression of Hxt2p. Under certain growth conditions, over-expression of SKS1 itself leads to a growth defect which is diminished in snf3 hxt2 double mutants. This suggests that over-expression of Hxt2p at physiologically inappropriate times is detrimental to the cells.
SKS1基因最初被鉴定为在低葡萄糖浓度下snf3缺失突变体生长缺陷的多拷贝抑制子。Snf3p在低底物浓度生长期间快速诱导HXT2是必需的。Snf3p的缺失导致HXT2表达显著延迟。在snf3 sks1双缺失突变体菌株中不会发生对低底物浓度的适应，这表明在缺乏Snf3p活性的情况下，SKS1是HXT2葡萄糖依赖性表达所必需的。SKS1的过表达导致Hxt2p的过表达，从而解释了抑制snf3缺陷的机制。SKS1定义了一条独立于Snf3p的Hxt2p表达新途径。在某些生长条件下，SKS1自身的过表达导致生长缺陷，而在snf3 hxt2双突变体中这种缺陷会减轻。这表明在生理上不适当的时间过表达Hxt2p对细胞是有害的。
