Microprocessor, Setx, Xrn2, and Rrp6 Co-operate to Induce Premature Termination of Transcription by RNAPII

Alexandre Wagschal; Emilie Rousset; Poornima Basavarajaiah; Xavier Contreras; Alex Harwig; Sabine Laurent-Chabalier; Mirai Nakamura; Xin Chen; Ke Zhang; Oussama Meziane; Frédéric Boyer; Hugues Parrinello; Ben Berkhout; Christophe Terzian; Monsef Benkirane; Rosemary Kiernan

doi:https://doi.org/10.1016/j.cell.2012.08.004

Microprocessor, Setx, Xrn2, and Rrp6 Co-operate to Induce Premature Termination of Transcription by RNAPII

Alexandre Wagschal, Emilie Rousset, Poornima Basavarajaiah, Xavier Contreras, Alex Harwig, Sabine Laurent-Chabalier, Mirai Nakamura, Xin Chen, Ke Zhang, Oussama Meziane, Frédéric Boyer, Hugues Parrinello, Ben Berkhout, Christophe Terzian, Monsef Benkirane, Rosemary Kiernan

Medical Microbiology and Infection Prevention (AMC)

Research output: Contribution to journal › Article › Academic › peer-review

141 Citations (Scopus)

Abstract

Transcription elongation is increasingly recognized as an important mechanism of gene regulation. Here, we show that microprocessor controls gene expression in an RNAi-independent manner. Microprocessor orchestrates the recruitment of termination factors Setx and Xrn2, and the 30-50 exoribonuclease, Rrp6, to initiate RNAPII pausing and premature termination at the HIV-1 promoter through cleavage of the stem-loop RNA, TAR. Rrp6 further processes the cleavage product, which generates a small RNA that is required to mediate potent transcriptional repression and chromatin remodeling at the HIV-1 promoter. Using chromatin immunoprecipitation coupled to high-throughput sequencing (ChIP-seq), we identified cellular gene targets whose transcription is modulated by microprocessor. Our study reveals RNAPII pausing and premature termination mediated by the co-operative activity of ribonucleases, Drosha/Dgcr8, Xrn2, and Rrp6, as a regulatory mechanism of RNAPII-dependent transcription elongation

Original language	English
Pages (from-to)	1147-1157
Journal	Cell
Volume	150
Issue number	6
DOIs	https://doi.org/10.1016/j.cell.2012.08.004
Publication status	Published - 2012

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https://doi.org/10.1016/j.cell.2012.08.004

Cite this

Wagschal, A., Rousset, E., Basavarajaiah, P., Contreras, X., Harwig, A., Laurent-Chabalier, S., Nakamura, M., Chen, X., Zhang, K., Meziane, O., Boyer, F., Parrinello, H., Berkhout, B., Terzian, C., Benkirane, M., & Kiernan, R. (2012). Microprocessor, Setx, Xrn2, and Rrp6 Co-operate to Induce Premature Termination of Transcription by RNAPII. Cell, 150(6), 1147-1157. https://doi.org/10.1016/j.cell.2012.08.004

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title = "Microprocessor, Setx, Xrn2, and Rrp6 Co-operate to Induce Premature Termination of Transcription by RNAPII",

abstract = "Transcription elongation is increasingly recognized as an important mechanism of gene regulation. Here, we show that microprocessor controls gene expression in an RNAi-independent manner. Microprocessor orchestrates the recruitment of termination factors Setx and Xrn2, and the 30-50 exoribonuclease, Rrp6, to initiate RNAPII pausing and premature termination at the HIV-1 promoter through cleavage of the stem-loop RNA, TAR. Rrp6 further processes the cleavage product, which generates a small RNA that is required to mediate potent transcriptional repression and chromatin remodeling at the HIV-1 promoter. Using chromatin immunoprecipitation coupled to high-throughput sequencing (ChIP-seq), we identified cellular gene targets whose transcription is modulated by microprocessor. Our study reveals RNAPII pausing and premature termination mediated by the co-operative activity of ribonucleases, Drosha/Dgcr8, Xrn2, and Rrp6, as a regulatory mechanism of RNAPII-dependent transcription elongation",

author = "Alexandre Wagschal and Emilie Rousset and Poornima Basavarajaiah and Xavier Contreras and Alex Harwig and Sabine Laurent-Chabalier and Mirai Nakamura and Xin Chen and Ke Zhang and Oussama Meziane and Fr{\'e}d{\'e}ric Boyer and Hugues Parrinello and Ben Berkhout and Christophe Terzian and Monsef Benkirane and Rosemary Kiernan",

year = "2012",

doi = "https://doi.org/10.1016/j.cell.2012.08.004",

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Wagschal, A, Rousset, E, Basavarajaiah, P, Contreras, X, Harwig, A, Laurent-Chabalier, S, Nakamura, M, Chen, X, Zhang, K, Meziane, O, Boyer, F, Parrinello, H, Berkhout, B, Terzian, C, Benkirane, M & Kiernan, R 2012, 'Microprocessor, Setx, Xrn2, and Rrp6 Co-operate to Induce Premature Termination of Transcription by RNAPII', Cell, vol. 150, no. 6, pp. 1147-1157. https://doi.org/10.1016/j.cell.2012.08.004

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T1 - Microprocessor, Setx, Xrn2, and Rrp6 Co-operate to Induce Premature Termination of Transcription by RNAPII

AU - Wagschal, Alexandre

AU - Rousset, Emilie

AU - Basavarajaiah, Poornima

AU - Contreras, Xavier

AU - Harwig, Alex

AU - Laurent-Chabalier, Sabine

AU - Nakamura, Mirai

AU - Chen, Xin

AU - Zhang, Ke

AU - Meziane, Oussama

AU - Boyer, Frédéric

AU - Parrinello, Hugues

AU - Berkhout, Ben

AU - Terzian, Christophe

AU - Benkirane, Monsef

AU - Kiernan, Rosemary

PY - 2012

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AB - Transcription elongation is increasingly recognized as an important mechanism of gene regulation. Here, we show that microprocessor controls gene expression in an RNAi-independent manner. Microprocessor orchestrates the recruitment of termination factors Setx and Xrn2, and the 30-50 exoribonuclease, Rrp6, to initiate RNAPII pausing and premature termination at the HIV-1 promoter through cleavage of the stem-loop RNA, TAR. Rrp6 further processes the cleavage product, which generates a small RNA that is required to mediate potent transcriptional repression and chromatin remodeling at the HIV-1 promoter. Using chromatin immunoprecipitation coupled to high-throughput sequencing (ChIP-seq), we identified cellular gene targets whose transcription is modulated by microprocessor. Our study reveals RNAPII pausing and premature termination mediated by the co-operative activity of ribonucleases, Drosha/Dgcr8, Xrn2, and Rrp6, as a regulatory mechanism of RNAPII-dependent transcription elongation

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DO - https://doi.org/10.1016/j.cell.2012.08.004

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SN - 0092-8674

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JO - Cell

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