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泛素 E3 连接酶 STUB1 通过降解 CDK9 调控 P-TEFb 水平及其在哺乳动物细胞内对全基因组靶基因表达的功能。

Degradation of CDK9 by Ubiquitin E3 Ligase STUB1 Regulates P-TEFb Level and Its Functions for Global Target Gene Expression within Mammalian Cells.

机构信息

Laboratory of Transcription Biology, Molecular Genetics Division, CSIR-Indian Institute of Chemical Biology, Kolkata, India.

Academy of Scientific and Innovative Research (AcSIR), Ghaziabad, India.

出版信息

Mol Cell Biol. 2023;43(9):451-471. doi: 10.1080/10985549.2023.2239694. Epub 2023 Aug 11.

Abstract

Positive transcription elongation factor b (P-TEFb) regulates expression of diverse sets of genes within mammalian cells that have implications in several human disease pathogeneses. However, mechanisms of functional regulation of P-TEFb complex through regulation of its stability are poorly known. In this study, we show an important role of C-terminus of Hsc70-interacting protein (CHIP aka STUB1) in regulation of overall level of CDK9 and thus P-TEFb complex within mammalian cells. STUB1 acts as a ubiquitin E3 ligase for proteasomal degradation of CDK9 involving N-terminal lysine 3 (K3) residue. Whereas, overexpression of STUB1 enhances, its knockdown reduces overall CDK9 degradation kinetics within mammalian cells. Interestingly, owing to the same region of binding within CDK9, CyclinT1 protects CDK9 from STUB1-mediated degradation. Factors that cooperatively bind with CyclinT1 to form functional complex also protects CDK9 from degradation by STUB1. Knockdown of STUB1 enhances CDK9 expression and thus P-TEFb complex formation that leads to global increase in RNA polymerase II CTD phosphorylation and transcriptional activation of diverse P-TEFb target genes. Thus, we describe an important functional role of STUB1 in regulation of transcription through modulation of overall level of P-TEFb complex formation within mammalian cells.

摘要

正转录延伸因子 b(P-TEFb)调节哺乳动物细胞中多种基因的表达,这些基因在几种人类疾病的发病机制中具有重要意义。然而,通过调节 P-TEFb 复合物的稳定性来调节其功能的机制知之甚少。在这项研究中,我们表明 Hsc70 相互作用蛋白(CHIP 又名 STUB1)的 C 端在调节哺乳动物细胞中 CDK9 的整体水平和因此 P-TEFb 复合物方面起着重要作用。STUB1 作为一种泛素 E3 连接酶,通过涉及 N 端赖氨酸 3(K3)残基的蛋白酶体降解 CDK9。然而,STUB1 的过表达增强,其敲低降低了哺乳动物细胞中 CDK9 的整体降解动力学。有趣的是,由于 CDK9 结合的同一区域,CyclinT1 保护 CDK9 免受 STUB1 介导的降解。与 CyclinT1 协同结合形成功能性复合物的因子也可防止 CDK9 被 STUB1 降解。STUB1 的敲低增强了 CDK9 的表达,从而形成 P-TEFb 复合物,导致 RNA 聚合酶 II CTD 磷酸化的全局增加和各种 P-TEFb 靶基因的转录激活。因此,我们描述了 STUB1 在通过调节哺乳动物细胞中 P-TEFb 复合物形成的整体水平来调节转录方面的重要功能作用。

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