Transcription recycling assays identify PAF1 as a driver for RNA Pol II recycling.

Autor: Chen Z; Department of Pathology and Duke Cancer Institute, Duke University School of Medicine, Durham, NC, 27710, USA. zhong.chen128@duke.edu., Hankey W; Department of Pathology and Duke Cancer Institute, Duke University School of Medicine, Durham, NC, 27710, USA., Zhao Y; Department of Pathology and Duke Cancer Institute, Duke University School of Medicine, Durham, NC, 27710, USA.; Department of Pathology, College of Basic Medical Sciences and First Affiliated Hospital, China Medical University, Shenyang, 110122, China., Groth J; Department of Pathology and Duke Cancer Institute, Duke University School of Medicine, Durham, NC, 27710, USA., Huang F; Department of Pathology and Duke Cancer Institute, Duke University School of Medicine, Durham, NC, 27710, USA., Wang H; Department of Pathology and Duke Cancer Institute, Duke University School of Medicine, Durham, NC, 27710, USA., Campos AR; Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, 92037, USA., Huang J; Department of Pathology and Duke Cancer Institute, Duke University School of Medicine, Durham, NC, 27710, USA., Roeder RG; Laboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY, 10065, USA., Wang Q; Department of Pathology and Duke Cancer Institute, Duke University School of Medicine, Durham, NC, 27710, USA. qianben.wang@duke.edu.
Jazyk: angličtina
Zdroj: Nature communications [Nat Commun] 2021 Nov 03; Vol. 12 (1), pp. 6318. Date of Electronic Publication: 2021 Nov 03.
DOI: 10.1038/s41467-021-26604-1
Abstrakt: RNA Polymerase II (Pol II) transcriptional recycling is a mechanism for which the required factors and contributions to overall gene expression levels are poorly understood. We describe an in vitro methodology facilitating unbiased identification of putative RNA Pol II transcriptional recycling factors and quantitative measurement of transcriptional output from recycled transcriptional components. Proof-of-principle experiments identified PAF1 complex components among recycling factors and detected defective transcriptional output from Pol II recycling following PAF1 depletion. Dynamic ChIP-seq confirmed PAF1 silencing triggered defective Pol II recycling in human cells. Prostate tumors exhibited enhanced transcriptional recycling, which was attenuated by antibody-based PAF1 depletion. These findings identify Pol II recycling as a potential target in cancer and demonstrate the applicability of in vitro and cellular transcription assays to characterize Pol II recycling in other disease states.
(© 2021. The Author(s).)
Databáze: MEDLINE
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