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首页> 外文期刊>Molecular and Cellular Biology >Casein Kinase 2 Associates with Initiation-Competent RNA Polymerase I and Has Multiple Roles in Ribosomal DNA Transcription
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Casein Kinase 2 Associates with Initiation-Competent RNA Polymerase I and Has Multiple Roles in Ribosomal DNA Transcription

机译：酪蛋白激酶2与具有起始能力的RNA聚合酶I相关，并在核糖体DNA转录中具有多种作用

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摘要

Mammalian RNA polymerase I (Pol I) complexes contain a number of associated factors, some with undefined regulatory roles in transcription. We demonstrate that casein kinase 2 (CK2) in human cells is associated specifically only with the initiation-competent Pol Iβ isoform and not with Pol Iα. Chromatin immunoprecipitation analysis places CK2 at the ribosomal DNA (rDNA) promoter in vivo. Pol Iβ-associated CK2 can phosphorylate topoisomerase IIα in Pol Iβ, activator upstream binding factor (UBF), and selectivity factor 1 (SL1) subunit TAFI110. A potent and selective CK2 inhibitor, 3,8-dibromo-7-hydroxy-4-methylchromen-2-one, limits in vitro transcription to a single round, suggesting a role for CK2 in reinitiation. Phosphorylation of UBF by CK2 increases SL1-dependent stabilization of UBF at the rDNA promoter, providing a molecular mechanism for the stimulatory effect of CK2 on UBF activation of transcription. These positive effects of CK2 in Pol I transcription contrast to that wrought by CK2 phosphorylation of TAFI110, which prevents SL1 binding to rDNA, thereby abrogating the ability of SL1 to nucleate preinitiation complex (PIC) formation. Thus, CK2 has the potential to regulate Pol I transcription at multiple levels, in PIC formation, activation, and reinitiation of transcription.
机译：哺乳动物RNA聚合酶I（Pol I）复合物包含许多相关因素，其中一些在转录中具有不确定的调节作用。我们证明，人细胞中的酪蛋白激酶2（CK2）仅与具有启动能力的PolIβ亚型相关，而与PolIα不相关。染色质免疫沉淀分析在体内将CK2置于核糖体DNA（rDNA）启动子上。 PolIβ相关的CK2可以磷酸化PolIβ中的拓扑异构酶IIα，激活因子上游结合因子（UBF）和选择性因子1（SL1）亚基TAF I 110。一种有效且选择性的CK2抑制剂3,8-dibromo-7-hydroxy-4-methylchromen-2-one将体外转录限制在一个单轮，这表明CK2在重新初始化中起作用。 CK2对UBF的磷酸化增强了rDNA启动子处UBF的SL1依赖性稳定，为CK2对UBF转录激活的刺激作用提供了分子机制。 CK2在Pol I转录中的这些积极作用与TAF I 110的CK2磷酸化所产生的作用相反，后者阻止SL1与rDNA结合，从而消除了SL1形成预启动复合物（PIC）的能力。因此，CK2具有在PIC形成，激活和转录重新启动中在多个水平上调节Pol I转录的潜力。

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