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卡尔斯伯酵母果糖二磷酸酶突变体与6-磷酸果糖的无效循环

Saccharomyces carlsbergensis fdp mutant and futile cycling of fructose 6-phosphate.

作者信息

Bañuelos M, Fraenkel D G

出版信息

Mol Cell Biol. 1982 Aug;2(8):921-9. doi: 10.1128/mcb.2.8.921-929.1982.

Abstract

In Saccharomyces, the addition of glucose to cells grown in media lacking sugars causes irreversible inactivation of fructose bisphosphatase. One function of this process might be to prevent a futile cycle of formation and hydrolysis of fructose 1,6-bisphosphate. We tested such cycling by assessing the labeling of the 1-position of glucose in polysaccharides from [6-14C]glucose (J.P. Chambost and D. G. Fraenkel, J. Biol. Chem. 225:2867-2869, 1980) by using mutants impaired in glucose growth and known not to inactivate the phosphatase normally (i.e., the fdp mutant of Saccharomyces carlsbergensis [van de Poll et al., J. Bacteriol. 117:965-970, 1974] and the similar cif mutant of Saccharomyces cerevisiae [Navon et al., Biochemistry 18:4487-4499, 1979] ), as well as in the wild-type strain tested in the 1-h period before inactivation is complete. There was marginal, if any, cycling in any situation, and we conclude that the phosphatase activity is controlled by means other than inactivation or that the extent of cycling is too low to be significant, or both. For the fdp mutant data are also presented on growth, rate of glucose metabolism, metabolite accumulations, enzyme levels, and glucose transport, but the primary lesion is unknown.

摘要

在酿酒酵母中,向缺乏糖类的培养基中生长的细胞添加葡萄糖会导致果糖双磷酸酶不可逆失活。这一过程的一个功能可能是防止果糖1,6 -二磷酸形成和水解的无效循环。我们通过评估[6 - 14C]葡萄糖中多糖葡萄糖1位的标记情况(J.P. 尚博斯特和D.G. 弗伦克尔,《生物化学杂志》225:2867 - 2869,1980)来测试这种循环,使用的是在葡萄糖生长方面受损且已知不能正常使磷酸酶失活的突变体(即卡尔斯伯酵母的fdp突变体[范德波尔等人,《细菌学杂志》117:965 - 970,1974]和酿酒酵母类似的cif突变体[纳冯等人,《生物化学》18:4487 - 4499,1979]),以及在失活完成前1小时测试的野生型菌株。在任何情况下,循环都很微弱(如果有的话),我们得出结论,磷酸酶活性是通过失活以外的其他方式控制的,或者循环程度太低以至于不显著,或者两者皆是。对于fdp突变体,还给出了关于生长、葡萄糖代谢速率、代谢物积累、酶水平和葡萄糖转运的数据,但主要损伤尚不清楚。

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