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CTCF interacts with the lytic HSV-1 genome to promote viral transcription

CTCF is an essential chromatin regulator implicated in important nuclear processes including in nuclear organization and transcription. Herpes Simplex Virus-1 (HSV-1) is a ubiquitous human pathogen, which enters productive infection in human epithelial and many other cell types. CTCF is known to bin...

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Autores principales: Lang, Fengchao, Li, Xin, Vladimirova, Olga, Hu, Benxia, Chen, Guijun, Xiao, Yu, Singh, Vikrant, Lu, Danfeng, Li, Lihong, Han, Hongbo, Wickramasinghe, J. M. A. S. P., Smith, Sheryl T., Zheng, Chunfu, Li, Qihan, Lieberman, Paul M., Fraser, Nigel W., Zhou, Jumin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5206630/
https://www.ncbi.nlm.nih.gov/pubmed/28045091
http://dx.doi.org/10.1038/srep39861
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author Lang, Fengchao
Li, Xin
Vladimirova, Olga
Hu, Benxia
Chen, Guijun
Xiao, Yu
Singh, Vikrant
Lu, Danfeng
Li, Lihong
Han, Hongbo
Wickramasinghe, J. M. A. S. P.
Smith, Sheryl T.
Zheng, Chunfu
Li, Qihan
Lieberman, Paul M.
Fraser, Nigel W.
Zhou, Jumin
author_facet Lang, Fengchao
Li, Xin
Vladimirova, Olga
Hu, Benxia
Chen, Guijun
Xiao, Yu
Singh, Vikrant
Lu, Danfeng
Li, Lihong
Han, Hongbo
Wickramasinghe, J. M. A. S. P.
Smith, Sheryl T.
Zheng, Chunfu
Li, Qihan
Lieberman, Paul M.
Fraser, Nigel W.
Zhou, Jumin
author_sort Lang, Fengchao
collection PubMed
description CTCF is an essential chromatin regulator implicated in important nuclear processes including in nuclear organization and transcription. Herpes Simplex Virus-1 (HSV-1) is a ubiquitous human pathogen, which enters productive infection in human epithelial and many other cell types. CTCF is known to bind several sites in the HSV-1 genome during latency and reactivation, but its function has not been defined. Here, we report that CTCF interacts extensively with the HSV-1 DNA during lytic infection by ChIP-seq, and its knockdown results in the reduction of viral transcription, viral genome copy number and virus yield. CTCF knockdown led to increased H3K9me3 and H3K27me3, and a reduction of RNA pol II occupancy on viral genes. Importantly, ChIP-seq analysis revealed that there is a higher level of CTD Ser2P modified RNA Pol II near CTCF peaks relative to the Ser5P form in the viral genome. Consistent with this, CTCF knockdown reduced the Ser2P but increased Ser5P modified forms of RNA Pol II on viral genes. These results suggest that CTCF promotes HSV-1 lytic transcription by facilitating the elongation of RNA Pol II and preventing silenced chromatin on the viral genome.
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spelling pubmed-52066302017-01-04 CTCF interacts with the lytic HSV-1 genome to promote viral transcription Lang, Fengchao Li, Xin Vladimirova, Olga Hu, Benxia Chen, Guijun Xiao, Yu Singh, Vikrant Lu, Danfeng Li, Lihong Han, Hongbo Wickramasinghe, J. M. A. S. P. Smith, Sheryl T. Zheng, Chunfu Li, Qihan Lieberman, Paul M. Fraser, Nigel W. Zhou, Jumin Sci Rep Article CTCF is an essential chromatin regulator implicated in important nuclear processes including in nuclear organization and transcription. Herpes Simplex Virus-1 (HSV-1) is a ubiquitous human pathogen, which enters productive infection in human epithelial and many other cell types. CTCF is known to bind several sites in the HSV-1 genome during latency and reactivation, but its function has not been defined. Here, we report that CTCF interacts extensively with the HSV-1 DNA during lytic infection by ChIP-seq, and its knockdown results in the reduction of viral transcription, viral genome copy number and virus yield. CTCF knockdown led to increased H3K9me3 and H3K27me3, and a reduction of RNA pol II occupancy on viral genes. Importantly, ChIP-seq analysis revealed that there is a higher level of CTD Ser2P modified RNA Pol II near CTCF peaks relative to the Ser5P form in the viral genome. Consistent with this, CTCF knockdown reduced the Ser2P but increased Ser5P modified forms of RNA Pol II on viral genes. These results suggest that CTCF promotes HSV-1 lytic transcription by facilitating the elongation of RNA Pol II and preventing silenced chromatin on the viral genome. Nature Publishing Group 2017-01-03 /pmc/articles/PMC5206630/ /pubmed/28045091 http://dx.doi.org/10.1038/srep39861 Text en Copyright © 2017, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Lang, Fengchao
Li, Xin
Vladimirova, Olga
Hu, Benxia
Chen, Guijun
Xiao, Yu
Singh, Vikrant
Lu, Danfeng
Li, Lihong
Han, Hongbo
Wickramasinghe, J. M. A. S. P.
Smith, Sheryl T.
Zheng, Chunfu
Li, Qihan
Lieberman, Paul M.
Fraser, Nigel W.
Zhou, Jumin
CTCF interacts with the lytic HSV-1 genome to promote viral transcription
title CTCF interacts with the lytic HSV-1 genome to promote viral transcription
title_full CTCF interacts with the lytic HSV-1 genome to promote viral transcription
title_fullStr CTCF interacts with the lytic HSV-1 genome to promote viral transcription
title_full_unstemmed CTCF interacts with the lytic HSV-1 genome to promote viral transcription
title_short CTCF interacts with the lytic HSV-1 genome to promote viral transcription
title_sort ctcf interacts with the lytic hsv-1 genome to promote viral transcription
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5206630/
https://www.ncbi.nlm.nih.gov/pubmed/28045091
http://dx.doi.org/10.1038/srep39861
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