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细胞周期蛋白依赖性激酶对RNA聚合酶II转录的调控:结束之前不算完?

CDK regulation of transcription by RNAP II: Not over 'til it's over?

作者信息

Fisher Robert P

机构信息

a Department of Oncological Sciences , Icahn School of Medicine at Mount Sinai , New York , NY , USA.

出版信息

Transcription. 2017 Mar 15;8(2):81-90. doi: 10.1080/21541264.2016.1268244. Epub 2016 Dec 22.

DOI:10.1080/21541264.2016.1268244
PMID:28005463
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5423476/
Abstract

Transcription by RNA polymerase (RNAP) II is regulated at multiple steps by phosphorylation, catalyzed mainly by members of the cyclin-dependent kinase (CDK) family. The CDKs involved in transcription have overlapping substrate specificities, but play largely non-redundant roles in coordinating gene expression. Novel functions and targets of CDKs have recently emerged at the end of the transcription cycle, when the primary transcript is cleaved, and in most cases polyadenylated, and transcription is terminated by the action of the "torpedo" exonuclease Xrn2, which is a CDK substrate. Collectively, various functions have been ascribed to CDKs or CDK-mediated phosphorylation: recruiting cleavage and polyadenylation factors, preventing premature termination within gene bodies while promoting efficient termination of full-length transcripts, and preventing extensive readthrough transcription into intergenic regions or neighboring genes. The assignment of precise functions to specific CDKs is still in progress, but recent advances suggest ways in which the CDK network and RNAP II machinery might cooperate to ensure timely exit from the transcription cycle.

摘要

RNA聚合酶(RNAP)II的转录在多个步骤受到磷酸化的调控,主要由细胞周期蛋白依赖性激酶(CDK)家族成员催化。参与转录的CDK具有重叠的底物特异性,但在协调基因表达方面发挥着 largely 非冗余的作用。CDK的新功能和靶点最近出现在转录周期的末期,此时初级转录本被切割,并且在大多数情况下进行多聚腺苷酸化,转录通过“鱼雷”外切核酸酶Xrn2的作用终止,Xrn2是一种CDK底物。总的来说,CDK或CDK介导的磷酸化具有多种功能:招募切割和多聚腺苷酸化因子,防止基因体内的过早终止,同时促进全长转录本的有效终止,并防止广泛的通读转录进入基因间区域或相邻基因。将精确功能分配给特定CDK的工作仍在进行中,但最近的进展表明了CDK网络和RNAP II机制可能合作以确保及时退出转录周期的方式。

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