Disruption of the interaction between TFIIAαβ and TFIIA recognition element inhibits RNA polymerase II gene transcription in a promoter context-dependent manner.
Autor: | Wang J; School of Materials and Metallurgy, Wuhan University of Science and Technology, Wuhan 430081, China; College of Life Science and Health, Wuhan University of Science and Technology, Wuhan 430065, China., Shi K; College of Life Science and Health, Wuhan University of Science and Technology, Wuhan 430065, China., Wu Z; College of Life Science and Health, Wuhan University of Science and Technology, Wuhan 430065, China., Zhang C; College of Life Science and Health, Wuhan University of Science and Technology, Wuhan 430065, China., Li Y; College of Life Science and Health, Wuhan University of Science and Technology, Wuhan 430065, China., Deng H; College of Life Science and Health, Wuhan University of Science and Technology, Wuhan 430065, China., Zhao S; College of Life Science and Health, Wuhan University of Science and Technology, Wuhan 430065, China. Electronic address: zhaoshasha@wust.edu.cn., Deng W; College of Life Science and Health, Wuhan University of Science and Technology, Wuhan 430065, China. Electronic address: dengwensheng@wust.edu.cn. |
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Jazyk: | angličtina |
Zdroj: | Biochimica et biophysica acta. Gene regulatory mechanisms [Biochim Biophys Acta Gene Regul Mech] 2020 Oct; Vol. 1863 (10), pp. 194611. Date of Electronic Publication: 2020 Jul 31. |
DOI: | 10.1016/j.bbagrm.2020.194611 |
Abstrakt: | General transcription factors and core promoter elements play a pivotal role in RNA polymerase II (Pol II)-mediated transcription initiation. In the previous work, we have defined a TFIIA recognition element (IIARE) that modulates Pol II-directed gene transcription in a promoter context-dependent manner. However, how TFIIA interacts with the IIARE and whether the interaction between TFIIA and the IIARE is involved in the regulation of gene transcription by Pol II are not fully understood. In the present study, we confirm that both K348 and K350 residues in TFIIAαβ are required for the interaction between TFIIAαβ and the IIARE. Disruption of the interaction between them by gene mutations dampens TFIIAαβ binding to the AdML-IIARE promoter and the transcriptional activation of the promoter containing a IIARE in vitro and in vivo. Stable expression of the TFIIAαβ mutant containing both K348A and K350A in the cell line with endogenous TFIIAαβ silence represses endogenous gene expression by reducing the occupancies of TFIIAαβ, TBP, p300, and Pol II at the promoters containing a IIARE. The findings from this study provide a novel insight into the regulatory mechanism of gene transcription mediated by TFIIA and the IIARE. Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. (Copyright © 2020 Elsevier B.V. All rights reserved.) |
Databáze: | MEDLINE |
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