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在维持能量电荷期间大肠杆菌中糖原合成与葡萄糖利用的调控。糖原合成速率和葡萄糖利用速率的变化与6-磷酸葡萄糖和1,6-二磷酸果糖细胞水平的同时变化之间的定量相关性。

Regulation of glycogen synthesis and glucose utilization in Escherichia coli during maintenance of the energy charge. Quantitative correlation of changes in the rates of glycogen synthesis and glucose utilization with simultaneous changes in the cellular levels of both glucose 6-phosphate and fructose 1,6-diphosphate.

作者信息

Dietzler D N, Leckie M P, Sternheim W L, Ungar J M, Crimmins D L, Lewis J W

出版信息

J Biol Chem. 1979 Sep 10;254(17):8276-87.

PMID:381301
Abstract

Treatment of nitrogen-starved cultures of Escherichia coli W4597(K) with sodium azide results in simultaneous changes in both glucose 6-phosphate and fructose 1,6-diphosphate as well as in the rate of glycogen synthesis. Based on these observations, a comprehensive equation was developed which relates the cellular levels of both of these hexose phosphates with the rate of glycogen synthesis. This relationship apparently represents the interaction in vivo between the rate-limiting enzyme of bacterial glycogen synthesis, glucose 1-phosphate adenylyltransferase (adenosine diphosphoglucose synthetase, EC 2.7.7.27), and its substrate glucose 1-phosphate (reflected by glucose 6-phosphate) and its major allosteric activator fructose diphosphate. The form of the equation that describes this relationship was determined from studies presented here of the kinetic properties of the E. coli W4597(K) enzyme in the presence of physiological concentrations of its substrates and modulators. We show here and in subsequent reports of this series that the comprehensive relationship between glycogen synthesis and hexose phosphates can serve as a reference to evaluate the possible participation of new factors in the regulation of glycogen synthesis. Treatment with NaN3 did not change the cellular level of glucose 1-phosphate adenylyltransferase. The value of the adenylate energy charge, (ATP + 1/2 ADP)/(ATP + ADP + AMP), was maintained despite losses of up to 35% in cellular adenylates. The quantitative co-variance between hexose phosphates and the cellular rate of glucose utilization that we previously described for other metabolic conditions was also observed in the azide-treated cultures. We integrate the new information into the system of coordinated regulation of glycogen synthesis, glycolysis, and glucose utilization that we proposed previously.

摘要

用叠氮化钠处理大肠杆菌W4597(K)的缺氮培养物,会导致6-磷酸葡萄糖和1,6-二磷酸果糖同时发生变化,以及糖原合成速率改变。基于这些观察结果,推导出了一个综合方程,该方程将这两种己糖磷酸的细胞水平与糖原合成速率联系起来。这种关系显然代表了细菌糖原合成的限速酶1-磷酸葡萄糖腺苷酸转移酶(二磷酸腺苷葡萄糖合成酶,EC 2.7.7.27)与其底物1-磷酸葡萄糖(由6-磷酸葡萄糖反映)及其主要变构激活剂二磷酸果糖在体内的相互作用。描述这种关系的方程形式是根据此处关于大肠杆菌W4597(K)酶在其底物和调节剂生理浓度存在下的动力学性质的研究确定的。我们在此处以及本系列的后续报告中表明,糖原合成与己糖磷酸之间的综合关系可作为评估新因素可能参与糖原合成调节的参考。用NaN3处理不会改变1-磷酸葡萄糖腺苷酸转移酶的细胞水平。尽管细胞腺苷酸损失高达35%,腺苷酸能荷值(ATP + 1/2 ADP)/(ATP + ADP + AMP)仍保持不变。我们之前描述的其他代谢条件下己糖磷酸与细胞葡萄糖利用速率之间的定量协变关系,在叠氮化钠处理的培养物中也观察到了。我们将新信息整合到我们之前提出的糖原合成、糖酵解和葡萄糖利用的协调调节系统中。

相似文献

1
Regulation of glycogen synthesis and glucose utilization in Escherichia coli during maintenance of the energy charge. Quantitative correlation of changes in the rates of glycogen synthesis and glucose utilization with simultaneous changes in the cellular levels of both glucose 6-phosphate and fructose 1,6-diphosphate.在维持能量电荷期间大肠杆菌中糖原合成与葡萄糖利用的调控。糖原合成速率和葡萄糖利用速率的变化与6-磷酸葡萄糖和1,6-二磷酸果糖细胞水平的同时变化之间的定量相关性。
J Biol Chem. 1979 Sep 10;254(17):8276-87.
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Contribution of cyclic adenosine 3':5'-monophosphate to the regulation of bacterial glycogen synthesis in vivo. Effect of carbon source and cyclic adenosine 3':5'-monophosphate on the quantitative relationship between the rate of glycogen synthesis and the cellular concentrations of glucose 6-phosphate and fructose 1,6-diphosphate in Escherichia coli.环磷酸腺苷对体内细菌糖原合成调控的作用。碳源和环磷酸腺苷对大肠杆菌中糖原合成速率与6-磷酸葡萄糖和1,6-二磷酸果糖细胞浓度之间定量关系的影响。
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Evidence for the coordinate control of glycogen synthesis, glucose utilization, and glycolysis in Escherichia coli. II. Quantitative correlation of the inhibition of glycogen synthesis and the stimulation of glucose utilization by 2,4-dinitrophenol with the effects on the cellular levels of glucose 6-phosphate, fructose, 1,6-diphosphate, and total adenylates.大肠杆菌中糖原合成、葡萄糖利用和糖酵解协同调控的证据。II. 2,4-二硝基苯酚对糖原合成的抑制和对葡萄糖利用的刺激与对细胞内6-磷酸葡萄糖、果糖、1,6-二磷酸果糖及总腺苷酸水平的影响之间的定量关系。
J Biol Chem. 1975 Sep 25;250(18):7195-203.
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Evidence for new factors in the coordinate regulation of energy metabolism in Escherichia coli. Effects of hypoxia, chloramphenicol succinate, and 2,4-dinitrophenol on glucose utilization, glycogen synthesis, adenylate energy charge, and hexose phosphates during the first two periods of nitrogen starvation.大肠杆菌能量代谢协同调控新因子的证据。在氮饥饿的前两个阶段,缺氧、琥珀氯霉素和2,4-二硝基苯酚对葡萄糖利用、糖原合成、腺苷酸能荷及己糖磷酸的影响。
J Biol Chem. 1979 Sep 10;254(17):8295-307.
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Evidence for the coordinate control of glycogen synthesis, glucose utilization, and glycolysis in Escherichia coli. I. Quantitative covariance of the rate of glucose utilization and the cellular level of fructose 1,6-diphosphate during exponential growth and nutrient limitation.大肠杆菌中糖原合成、葡萄糖利用和糖酵解协同调控的证据。I. 指数生长和营养限制期间葡萄糖利用率与细胞内1,6-二磷酸果糖水平的定量协变关系。
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Biosynthesis of bacterial glycogen. Kinetic studies of a glucose-1-phosphate adenylyltransferase (EC 2.7.7.27) from a glycogen-deficient mutant of Escherichia coli B.细菌糖原的生物合成。来自大肠杆菌B糖原缺陷型突变体的葡萄糖-1-磷酸腺苷酰转移酶(EC 2.7.7.27)的动力学研究。
J Biol Chem. 1975 Oct 10;250(19):7631-8.
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Evidence for the allosteric regulation of glycogen synthesis in the intact Escherichia coli cell. Agreement of the values of the parameters of the Hill equation fitted to data for glycogen synthesis in vivo with the abailable values obtained in vitro with adenosine diphosphoglucose synthetase.完整大肠杆菌细胞中糖原合成变构调节的证据。将希尔方程参数值与体内糖原合成数据拟合,所得结果与用二磷酸腺苷葡萄糖合成酶体外获得的现有值相符。
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Prediction of the rate of glucose utilization from cellular levels of glucose 6-phosphate and fructose 1,6-diphosphate in Escherichia coli.基于大肠杆菌中6-磷酸葡萄糖和1,6-二磷酸果糖的细胞水平预测葡萄糖利用速率
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Simultaneous increases of the adenylate energy charge and the rate of glycogen synthesis in nitrogen-starved Escherichia coli W4597(K).在氮饥饿的大肠杆菌W4597(K)中,腺苷酸能量电荷和糖原合成速率同时增加。
Arch Biochem Biophys. 1974 Jan;160(1):14-25. doi: 10.1016/s0003-9861(74)80003-2.

引用本文的文献

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