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Artificial RNA Polymerase II Elongation Complexes for Dissecting Co-transcriptional RNA Processing Events
Published on: May 13, 2019
ELL facilitates RNA polymerase II pause site entry and release
Jung S Byun1, Temesgen D Fufa, Clay Wakano
1Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, Bethesda, Maryland 20892, USA.
The eleven-nineteen lysine-rich leukaemia (ELL) protein stabilizes RNA polymerase II recruitment and initiation, crucial for gene activation. Loss of ELL disrupts early gene expression, impacting transcriptional activation of rapidly induced genes.
Area of Science:
- Molecular Biology
- Gene Regulation
- Biochemistry
Background:
- Transcription is a complex, multi-step process involving RNA polymerase II (Pol II).
- The super elongation complex (SEC) regulates transcriptional elongation.
- The eleven-nineteen lysine-rich leukaemia (ELL) protein is a component of the SEC.
Purpose of the Study:
- To investigate the role of ELL in transcription beyond its function in the SEC.
- To determine ELL's specific contributions to Pol II recruitment, initiation, and early elongation.
- To understand ELL's impact on the transcriptional activation of rapidly induced genes.
Main Methods:
- Investigated the function of ELL in stabilizing pre-initiation complexes.
- Assessed the effects of ELL loss on Pol II recruitment, initiation, and pause site entry.
- Analyzed chromatin structure and gene expression changes following ELL depletion.
Main Results:
- ELL stabilizes Pol II recruitment/initiation and facilitates entry into the pause site.
- Loss of ELL destabilizes pre-initiation complexes and disrupts early elongation.
- ELL depletion impairs promoter proximal chromatin structure and reduces activation of rapidly induced genes.
Conclusions:
- ELL plays an essential, early role in transcriptional regulation preceding its assembly into the SEC.
- ELL is critical for Pol II pause site entry and release, vital for high-amplitude gene expression.
- ELL's function is indispensable for rapid transcriptional responses.
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