Alterations of the glucose metabolism in a triose phosphate isomerase-negative Saccharomyces cerevisiae mutant
Alterations of the glucose metabolism in a triose phosphate isomerase-negative Saccharomyces cerevisiae mutant
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作者：
Campagno, C;Brambilla, L;Porro, D
磷酸丙糖异构酶活性的缺乏导致两种丙糖中仅一种（磷酸二羟丙酮）的积累，并且这产生葡萄糖催化剂的最终产物从乙醇到甘油的转变（Compagno等人，1996），在分批和连续培养中研究了由酿酒酵母中TPI 1基因缺失引起的葡萄糖代谢的改变。Δ tpi 1无效突变体不能在葡萄糖作为唯一碳源上生长。在含有葡萄糖的培养基中加入乙醇或乙酸盐，但也含有棉子糖或半乳糖，在分批培养中减轻了这种效应，表明克拉布特里效应不是突变体在葡萄糖上生长受损的主要原因。添加能量源如甲酸恢复了葡萄糖的利用，这表明Delta tpi 1突变体中的NADH/能量短缺可能是葡萄糖生长受损的原因。Δ tpi 1突变体中甘油产生的量可以代表通过糖酵解引导的碳源的分数的良好指标。在混合底物上连续培养获得的数据表明，糖酵解和糖异生以及HMP途径对Delta tpi 1突变体葡萄糖利用的不同贡献可能与培养基中存在的乙醇分数有关。版权所有（C）2001约翰威利父子有限公司
The absence of triose phosphate isomerase activity causes an accumulation of only one of the two trioses, dihydroxyacetone phosphate, and this produces a shift in the final product of glucose catabolism from ethanol to glycerol (Compagno et al., 1996), Alterations of glucose metabolism imposed by the deletion of the TPI1 gene in Saccharomyces,cerevisiae were studied in batch and continuous cultures. The Delta tpi1 null mutant was unable to grow on glucose as the sole carbon source. The addition of ethanol or acetate in media containing glucose, but also raffinose or galactose, relieved this effect in batch cultivation, suggesting that the Crabtree effect is not the primary cause for the mutant's impaired growth on glucose. The addition of an energy source like formic acid restored glucose utilization, suggesting that a NADH/energy shortage in the Delta tpi1 mutant could be a cause of the impaired growth on glucose. The amount of glycerol production in the Delta tpi1 mutant could represent a good indicator of the fraction of carbon source channelled through glycolysis. Data obtained in continuous cultures on mixed substrates indicated that different contributions of glycolysis and gluconeogenesis, as well as of the HMP pathway, to glucose utilization by the Delta tpi1 mutant may occur in relation to the fraction of ethanol present in the media. Copyright (C) 2001 John Wiley & Sons, Ltd.