The NIMA protein kinase is hyperphosphorylated and activated downstream of p34cdc2/cyclin B: coordination of two mitosis promoting kinases.
The NIMA protein kinase is hyperphosphorylated and activated downstream of p34cdc2/cyclin B: coordination of two mitosis promoting kinases.
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NIMA 蛋白激酶在 p34cdc2/cyclin B 下游过度磷酸化并被激活：两个有丝分裂促进激酶的协调。
DOI：
10.1002/j.1460-2075.1995.tb07079.x
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Osmani,SA
中科院分区：
文献类型：
--
作者：
Ye,XS;Xu,G;Pu,RT;Fincher,RR;McGuire,SL;Osmani,AH;Osmani,SA
构巢曲霉有丝分裂的启动需要两种蛋白激酶p34 cdc 2/cyclin B和NIMA的激活。即使p34 cdc 2失活，NIMA的强制表达也会促进染色质凝聚。因此，NIMA可能直接引起有丝分裂染色体凝聚。然而，NIMA的有丝分裂促进功能通常在p34 cdc 2/细胞周期蛋白B的控制下，因为当细胞启动有丝分裂时，NIMA的活性G2形式被过度磷酸化并被p34 cdc 2/细胞周期蛋白B进一步激活。为了观察NIMA的p34 cdc 2/细胞周期蛋白B依赖性活化，必须将冈田酸加入到分离缓冲液中以防止分离期间NIMA的去磷酸化。过度磷酸化的NIMA含有MPM-2表位，并且在体外，通过p34 cdc 2/细胞周期蛋白B磷酸化NIMA产生MPM-2表位，表明NIMA在有丝分裂起始期间直接通过p34 cdc 2/细胞周期蛋白B磷酸化。这两种激酶都是有丝分裂起始所必需的，因此在G2期作为蛋白激酶被独立激活。然后，为了启动有丝分裂，我们建议每一个都激活另一个的有丝分裂促进功能。这确保了细胞协调激活p34 cdc 2/细胞周期蛋白B和NIMA，以仅在完成所有间期事件后启动有丝分裂。最后，我们表明，NIMA是通过细胞周期调控，如细胞周期蛋白B，因为它积累在G2期，只有当细胞穿越有丝分裂降解。
Initiation of mitosis in Aspergillus nidulans requires activation of two protein kinases, p34cdc2/cyclin B and NIMA. Forced expression of NIMA, even when p34cdc2 was inactivated, promoted chromatin condensation. NIMA may therefore directly cause mitotic chromosome condensation. However, the mitosis‐promoting function of NIMA is normally under control of p34cdc2/cyclin B as the active G2 form of NIMA is hyperphosphorylated and further activated by p34cdc2/cyclin B when cells initiate mitosis. To see the p34cdc2/cyclin B dependent activation of NIMA, okadaic acid had to be added to isolation buffers to prevent dephosphorylation of NIMA during isolation. Hyperphosphorylated NIMA contained the MPM‐2 epitope and, in vitro, phosphorylation of NIMA by p34cdc2/cyclin B generated the MPM‐2 epitope, suggesting that NIMA is phosphorylated directly by p34cdc2/cyclin B during mitotic initiation. These two kinases, which are both essential for mitotic initiation, are therefore independently activated as protein kinases during G2. Then, to initiate mitosis, we suggest that each activates the other's mitosis‐promoting functions. This ensures that cells coordinately activate p34cdc2/cyclin B and NIMA to initiate mitosis only upon completion of all interphase events. Finally, we show that NIMA is regulated through the cell cycle like cyclin B, as it accumulates during G2 and is degraded only when cells traverse mitosis.