Evidence for phosphorylation/dephosphorylation control of phosphofructokinase from organs of the anoxia-tolerant sea mussel Mytilus edulis
Evidence for phosphorylation/dephosphorylation control of phosphofructokinase from organs of the anoxia-tolerant sea mussel Mytilus edulis
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耐缺氧海贻贝器官中磷酸果糖激酶磷酸化/去磷酸化控制的证据
DOI：
--
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
K. Storey
中科院分区：
文献类型：
--
作者：
B. Michaelidis;K. Storey
从有氧到缺氧的转变导致海洋双壳软体动物紫贻贝(Mytilus edulis L.)后收肌和肝胰腺的6-磷酸果糖-1-激酶(PFK)的动力学和调节特性发生稳定的改变，导致PFK的最大活性降低，对果糖-6-P的亲和力降低(S0.5在肌肉中增加60%，在肝胰腺中增加一倍)，激活剂(AMP，果糖-2，6-P2)的作用减弱，ATP的抑制作用减少(I50增加2-2.4倍)。酶激活剂在PFK性质上的器官特异性差异最大，肝胰腺酶对AMP和果糖-2，6-P2的Ka值要低得多，而且被无机磷酸盐激活(Ka 0.07 mM需氧，0.11 mM缺氧)。相比之下，PI对肌肉酶无影响，柠檬酸对两种酶均无抑制作用。为了确定缺氧诱导的PFK修饰是否是由于酶蛋白的共价修饰，将PFK样品与ATP+镁离子蛋白激酶第二信使(cAMP、cGMP或钙+佛波酯12-肉豆蔻酸盐13-醋酸酯)或与镁离子碱性磷酸酶孵育。蛋白激酶作用于后内收肌，增加了酶Vmax和对果糖-6-P的亲和力。CAMP或cGMP刺激的蛋白激酶对肝胰腺PFK具有相同的作用，但与蛋白激酶C刺激物孵育对该酶的作用相反。碱性磷酸酶处理逆转了体外磷酸化的影响。这些数据表明，在这些兼性厌氧菌向缺氧过渡过程中发生的糖酵解率抑制(反向巴斯德效应)是通过对PFK活性的可逆磷酸化控制来促进的。
The transition from aerobic to anoxic conditions induced stable modifications of the kinetic and regulatory properties of 6-phosphofructo-1-kinase (PFK) from the posterior adductor muscle and hepatopancreas of the marine bivalve mollusc Mytilus edulis L. Anoxia resulted in a reduction in the maximal activity of PFK, a decrease in affinity for fructose-6-P (S0.5 increased by 60% in muscle and twofold in hepatopancreas), reduced effects of activators (AMP, fructose-2,6-P2), and reduced inhibition by ATP (I50 increased 2–2.4 fold). Organ-specific differences in PFK properties were greatest for enzyme activators, with the hepatopancreas enzyme showing much lower Ka values for AMP and fructose-2,6-P2 as well as activation by inorganic phosphate (Ka 0.07 mM aerobic, 0.11 mM anoxic). By contrast, the muscle enzyme was not affected by Pi and neither enzyme was inhibited by citrate. To determine if the anoxia-induced modifications of PFK were due to covalent modification of the enzyme protein, PFK preparations were incubated with ATP + Mg2+ + protein kinase second messengers (cAMP, cGMP, or Ca2+ plus phorbol 12-myristate 13-acetate) or with Mg2+ + alkaline phosphatase. Protein kinase action on posterior adductor muscle PFK increased enzyme Vmax, and affinity for fructose-6-P. cAMP- or cGMP-stimulated protein kinase had the same action on hepatopancreas PFK; but incubation with stimulators of protein kinase C had the opposite effect on the enzyme. Alkaline phosphatase treatment reversed the effects of in vitro phosphorylation. The data suggest that the glycolytic rate depression (reverse Pasteur effect) that occurs with the transition to anoxia in these facultative anaerobes is facilitated by reversible phosphorylation control over the activity of PFK.
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影响因子：
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作者：
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DOI：
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DOI：
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发表时间：
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DOI：
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发表时间：
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期刊：
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作者：
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