THE MUTATION DGT1-1 DECREASES GLUCOSE-TRANSPORT AND ALLEVIATES CARBON CATABOLITE REPRESSION IN SACCHAROMYCES-CEREVISIAE

THE MUTATION DGT1-1 DECREASES GLUCOSE-TRANSPORT AND ALLEVIATES CARBON CATABOLITE REPRESSION IN SACCHAROMYCES-CEREVISIAE
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DOI:
10.1128/jb.176.24.7423-7429.1994
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发表时间:
1994-12-01
影响因子:
3.2
通讯作者:
GANCEDO, C
GANCEDO, C
中科院分区:
生物学3区
文献类型:
--
作者:
GAMO, FJ;LAFUENTE, MJ;GANCEDO, C

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乙醇-甘油混合物中的葡萄糖抑制缺乏磷酸甘油酸变位酶的酿酒酵母突变体的生长。分离出缓解葡萄糖抑制的抑制突变。这种突变 DGT1-1(减少葡萄糖转运)占主导地位,即使在野生型背景下也能产生多效性效应。 DGT1-1 突变体在葡萄糖中的生长依赖于呼吸作用,并且在添加葡萄糖后 7 小时内,在培养基中未检测到乙醇。当在葡萄糖上生长时,突变体的葡萄糖摄取减少,低亲和力和高亲和力运输系统都受到影响。在半乳糖生长的细胞中,仅检测到高亲和力葡萄糖转运系统。该系统在野生型和突变体中具有相似的动力学特征。在葡萄糖中生长期间,突变体不存在对几种酶的分解代谢物抑制,但在半乳糖中生长期间则不存在。与野生型相比,在葡萄糖中生长的突变体具有葡萄糖转运蛋白基因SNF3的高转录,而HXT1和HTX3没有转录。携带HXT1、HXT2或HXT3基因的多拷贝质粒的表达使得突变体的发酵能力和分解代谢物抑制部分恢复。结果表明,DGT1 编码葡萄糖转运基因表达的调节因子。他们还表明,葡萄糖通量可能决定作为分解代谢抑制信号的分子水平。
Glucose in ethanol-glycerol mixtures inhibits growth of Saccharomyces cerevisiae mutants lacking phosphoglycerate mutase. A suppressor mutation that relieved glucose inhibition was isolated. This mutation, DGT1-1 (decreasing glucose transport), was dominant and produced pleiotropic effects even in an otherwise wild-type background. Growth of the DGT1-1 mutant in glucose was dependent on respiration, and no ethanol was detected in the medium within 7 h of glucose addition. When grown on glucose, the mutant had a reduced glucose uptake and both the low- and high-affinity transport systems were affected. In galactose-grown cells, only the high-affinity glucose transport system was detected. This system had similar kinetic characteristics in the wild type and in the mutant. Catabolite repression of several enzymes was absent in the mutant during growth in glucose but not during growth in galactose. In contrast with the wild type, the mutant grown in glucose had high transcription of the glucose transporter gene SNF3 and no transcription of HXT1 and HTX3. Expression of multicopy plasmids carrying the HXT1, HXT2, or HXT3 gene allowed partial recovery of both fermentative capacity and catabolite repression in the mutant. The results suggest that DGT1 codes for a regulator of the expression of glucose transport genes. They also suggest that glucose flux might determine the levels of molecules implicated as signals in catabolite repression.