Eyer J, Leterrier J F
Centre de Neurochimie du C.N.R.S., Strasbourg, France.
Biochem J. 1988 Jun 15;252(3):655-60. doi: 10.1042/bj2520655.
The extensive enzymic dephosphorylation of neurofilaments determined the progressive loss of their capacity to interconnect in vitro into a reticulated network, measured by the formation of highly viscous gels in purified preparations of neurofilaments [Leterrier & Eyer (1987) Biochem. J. 245, 93-101]. Conversely, a cyclic AMP-dependent activation of the gelation process was obtained by phosphorylation of the neurofilament proteins by the cyclic-nucleotide-dependent protein kinase added to the preparation. These findings argue for a direct relationship between the high phosphorylation level of the neurofilament subunits and the cross-bridging of the polymers in vitro. However, a transient stimulation of the neurofilament viscosity kinetics was also observed during the early steps of dephosphorylation with acid phosphatase, which, moreover, disappeared with longer incubation times before the net inhibition was obtained. In the same way, the calmodulin-dependent brain phosphatase, calcineurin, induced a permanent activation of the phenomenon, correlated with a low dephosphorylation capacity of the neurofilament molecules. Taken together, these results suggest a functional heterogeneity of the numerous phosphate groups of the neurofilament subunits and raise the hypothesis of a highly controlled regulation of the neurofilament cross-bridging by selective phosphorylation-dephosphorylation mechanisms.
神经丝蛋白广泛的酶促去磷酸化决定了其在体外相互连接形成网状网络能力的逐渐丧失,这通过在纯化的神经丝蛋白制剂中形成高粘性凝胶来衡量[勒泰里耶与艾耶(1987年),《生物化学杂志》245卷,93 - 101页]。相反,通过向制剂中添加环核苷酸依赖性蛋白激酶使神经丝蛋白磷酸化,可获得环磷酸腺苷依赖性的凝胶化过程激活。这些发现表明神经丝亚基的高磷酸化水平与聚合物在体外的交联之间存在直接关系。然而,在用酸性磷酸酶去磷酸化的早期阶段,也观察到神经丝粘度动力学的短暂刺激,而且在获得净抑制之前,随着孵育时间延长这种刺激消失了。同样,钙调蛋白依赖性脑磷酸酶(钙神经素)诱导了该现象的永久激活,这与神经丝分子的低去磷酸化能力相关。综上所述,这些结果表明神经丝亚基众多磷酸基团存在功能异质性,并提出了通过选择性磷酸化 - 去磷酸化机制对神经丝交联进行高度可控调节的假说。