scholarly journals RNA Polymerase II Transcription Elongation Control

2013 ◽  
Vol 113 (11) ◽  
pp. 8583-8603 ◽  
Author(s):  
Jiannan Guo ◽  
David H. Price
2002 ◽  
Vol 10 (5) ◽  
pp. 1139-1150 ◽  
Author(s):  
Bernhard Dichtl ◽  
Diana Blank ◽  
Martin Ohnacker ◽  
Arno Friedlein ◽  
Daniel Roeder ◽  
...  

2016 ◽  
Vol 428 (12) ◽  
pp. 2623-2635 ◽  
Author(s):  
Tassa Saldi ◽  
Michael A. Cortazar ◽  
Ryan M. Sheridan ◽  
David L. Bentley

1997 ◽  
Vol 17 (10) ◽  
pp. 5791-5802 ◽  
Author(s):  
G G Parsons ◽  
C A Spencer

Nuclear RNA synthesis is repressed during the mitotic phase of each cell cycle. Although total RNA synthesis remains low throughout mitosis, the degree of RNA polymerase II transcription repression on specific genes has not been examined. In addition, it is not known whether mitotic repression of RNA polymerase II transcription is due to polymerase pausing or ejection of transcription elongation complexes from mitotic chromosomes. In this study, we show that RNA polymerase II transcription is repressed in mammalian cells on a number of specific gene regions during mitosis. We also show that the majority of RNA polymerase II transcription elongation complexes are physically excluded from mitotic chromosomes between late prophase and late telophase. Despite generalized transcription repression and stripping of RNA polymerase II complexes from DNA, arrested RNA polymerase II ternary complexes appear to remain on some gene regions during mitosis. The cyclic repression of transcription and ejection of RNA polymerase II transcription elongation complexes may help regulate the transcriptional events that control cell cycle progression and differentiation.


2018 ◽  
Vol 49 ◽  
pp. 54-62 ◽  
Author(s):  
Ilona Christy Unarta ◽  
Lizhe Zhu ◽  
Carmen Ka Man Tse ◽  
Peter Pak-Hang Cheung ◽  
Jin Yu ◽  
...  

2020 ◽  
Vol 48 (14) ◽  
pp. 7712-7727
Author(s):  
Michael Tellier ◽  
Justyna Zaborowska ◽  
Livia Caizzi ◽  
Eusra Mohammad ◽  
Taras Velychko ◽  
...  

Abstract Cyclin-dependent kinase 12 (CDK12) phosphorylates the carboxyl-terminal domain (CTD) of RNA polymerase II (pol II) but its roles in transcription beyond the expression of DNA damage response genes remain unclear. Here, we have used TT-seq and mNET-seq to monitor the direct effects of rapid CDK12 inhibition on transcription activity and CTD phosphorylation in human cells. CDK12 inhibition causes a genome-wide defect in transcription elongation and a global reduction of CTD Ser2 and Ser5 phosphorylation. The elongation defect is explained by the loss of the elongation factors LEO1 and CDC73, part of PAF1 complex, and SPT6 from the newly-elongating pol II. Our results indicate that CDK12 is a general activator of pol II transcription elongation and indicate that it targets both Ser2 and Ser5 residues of the pol II CTD.


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