Leckie M P, Ng R H, Porter S E, Compton D R, Dietzler D N
J Biol Chem. 1983 Mar 25;258(6):3813-24.
In Escherichia coli cya mutants, deficient in adenylate cyclase (EC 4.6.1.1), basal cellular rates of glycogen synthesis were lower and the relative increases produced by exogenous cyclic adenosine 3',5'-monophosphate during growth on glucose were greater than in their respective parent strains. These observations provide strong evidence that endogenous cyclic AMP is one of the key regulators of glycogen synthesis in growing E. coli. In crp mutants, deficient in cyclic AMP receptor protein (CRP), the basal cellular rates of glycogen synthesis were much lower than in their respective parent strains. Stimulation of glycogen synthesis by exogenous cyclic AMP was markedly attenuated in the three crp mutants. Thus, stimulation of glycogen synthesis by either endogenous or exogenous cyclic AMP appears to require CRP. Functional CRP appeared to be required for all three responses observed after cyclic AMP addition: an abrupt step-up in the cellular rate of glycogen synthesis, a continuing exponential increase in rate, and a stimulation of the rate during a subsequent nitrogen starvation. To account for these responses, we derived a mathematical model in which the cyclic AMP-CRP complex regulates the differential rate of synthesis of an enzyme metabolizing an effector of the rate-limiting enzyme of glycogen synthesis.
在缺乏腺苷酸环化酶（EC 4.6.1.1）的大肠杆菌cya突变体中，糖原合成的基础细胞速率较低，并且在葡萄糖上生长期间，外源性3',5'-环腺苷酸所产生的相对增加量大于其各自的亲本菌株。这些观察结果提供了强有力的证据，表明内源性环磷酸腺苷是生长中的大肠杆菌中糖原合成的关键调节因子之一。在缺乏环磷酸腺苷受体蛋白（CRP）的crp突变体中，糖原合成的基础细胞速率远低于其各自的亲本菌株。在三个crp突变体中，外源性环磷酸腺苷对糖原合成的刺激作用明显减弱。因此，内源性或外源性环磷酸腺苷对糖原合成的刺激似乎都需要CRP。功能性CRP似乎是添加环磷酸腺苷后观察到的所有三种反应所必需的：糖原合成细胞速率的突然跃升、速率的持续指数增加以及随后氮饥饿期间速率的刺激。为了解释这些反应，我们推导了一个数学模型，其中环磷酸腺苷-CRP复合物调节代谢糖原合成限速酶效应物的酶的差异合成速率。
