Dickinson J R, Sobanski M A, Hewlins M J
School of Pure and Applied Biology, University of Wales College of Cardiff, UK.
Microbiology (Reading). 1995 Feb;141 ( Pt 2):385-91. doi: 10.1099/13500872-141-2-385.
Saccharomyces cerevisiae mutants defective in the structural gene PGI1 lack phosphoglucose isomerase and hence cannot grow on glucose. Spontaneous mutants were isolated by selecting for the regained ability to grow on YEPD (yeast extract/peptone/glucose). Three complementation groups called spg29-31 (suppressor of pgi1 delta) were identified. The metabolism of [2-13C]glucose was studied by 13C NMR spectroscopy. This led to the conclusion that in a spg29 mutant suppression of the glycolytic defect was achieved by increased carbon flux through the hexose monophosphate pathway. The specific activities of enzymes of the hexose monophosphate pathway (except glucose-6-phosphate dehydrogenase) and NAD- and NADP-dependent glutamate dehydrogenase were increased in the bypass mutant.
酿酒酵母中结构基因PGI1有缺陷的突变体缺乏磷酸葡萄糖异构酶，因此无法在葡萄糖上生长。通过选择在YEPD（酵母提取物/蛋白胨/葡萄糖）上恢复生长的能力来分离自发突变体。鉴定出了三个互补组，称为spg29 - 31（pgi1δ的抑制子）。通过¹³C核磁共振光谱研究了[2 - ¹³C]葡萄糖的代谢。由此得出结论，在spg29突变体中，通过增加通过磷酸戊糖途径的碳通量实现了对糖酵解缺陷的抑制。在旁路突变体中，磷酸戊糖途径的酶（葡萄糖-6-磷酸脱氢酶除外）以及NAD和NADP依赖性谷氨酸脱氢酶的比活性增加。
