Cdc37 is essential for chromosome segregation and cytokinesis in higher eukaryotes
Cdc37 is essential for chromosome segregation and cytokinesis in higher eukaryotes
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DOI：
10.1093/emboj/cdf531
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发表时间：
2002-10-15
期刊：
影响因子：
11.4
通讯作者：
González, C
中科院分区：
文献类型：
--
作者：
Lange, BMH;Rebollo, E;González, C
CDC37已被证明是调节细胞周期进程不同阶段的蛋白激酶的活性和稳定性所必需的。然而，到目前为止，人们对CDC37与在细胞分裂中发挥作用的激酶的相互作用知之甚少。在这里，我们表明，在果蝇中，CDC37功能的丧失会导致有丝分裂和雄性减数分裂的缺陷，这些表型与Aurora B失活所带来的表型非常相似。我们提供了Aurora B与CDC37/Hsp90复合体相互作用的证据，并需要CDC37/Hsp90复合体来维持其稳定性。我们的结论是，CDC37/Hsp90复合体调节Aurora B的功能，并且CDC37功能丧失带来的大多数表型可以用该激酶的失活来解释。这些观察证实了CDC37作为关键细胞周期蛋白激酶的上游调控元件的作用。
Cdc37 has been shown to be required for the activity and stability of protein kinases that regulate different stages of cell cycle progression. However, little is known so far regarding interactions of Cdc37 with kinases that play a role in cell division. Here we show that the loss of function of Cdc37 in Drosophila leads to defects in mitosis and male meiosis, and that these phenotypes closely resemble those brought about by the inactivation of Aurora B. We provide evidence that Aurora B interacts with and requires the Cdc37/Hsp90 complex for its stability. We conclude that the Cdc37/Hsp90 complex modulates the function of Aurora B and that most of the phenotypes brought about by the loss of Cdc37 function can be explained by the inactivation of this kinase. These observations substantiate the role of Cdc37 as an upstream regulatory element of key cell cycle kinases.