Imperial College London
Portrait Picture

ProfessorPaulFarrell

Faculty of Medicine, Department of Infectious Disease

Professor of Tumour Virology
 
 
 
//

Contact

 

+44 (0)20 7594 2005p.farrell Website

 
 
//

Location

 

Section of VirologyNorfolk PlaceSt Mary's Campus

//

Summary

 

Publications

Citation

BibTex format

@article{Farrell:2019:nar/gky1323,
author = {Farrell, P and Paschos, K},
doi = {nar/gky1323},
journal = {Nucleic Acids Research},
pages = {2807--2821},
title = {Requirement for PRC1 subunit BMI1 in host gene activation by Epstein-Barr virus potein EBNA3C},
url = {http://dx.doi.org/10.1093/nar/gky1323},
volume = {47},
year = {2019}
}
Download

RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Epstein–Barr virus proteins EBNA3A, EBNA3B and EBNA3C control hundreds of host genes after infection. Changes in epigenetic marks around EBNA3-regulated genes suggest that they exert transcriptional control in collaboration with epigenetic factors. The roles of polycomb repressive complex (PRC)2 subunit SUZ12 and of PRC1 subunit BMI1 were assessed for their importance in EBNA3-mediated repression and activation. ChIP-seq experiments for SUZ12 and BMI1 were performed to determine their global localization on chromatin and analysis offered further insight into polycomb protein distribution in differentiated cells. Their localization was compared to that of each EBNA3 to resolve longstanding questions about the EBNA3–polycomb relationship. SUZ12 did not co-localize with any EBNA3, whereas EBNA3C co-localized significantly and co-immunoprecipitated with BMI1. In cells expressing a conditional EBNA3C, BMI1 was sequestered to EBNA3C-binding sites after EBNA3C activation. When SUZ12 or BMI1 was knocked down in the same cells, SUZ12 did not contribute to EBNA3C-mediated regulation. Surprisingly, after BMI1 knockdown, EBNA3C repressed equally efficiently but host gene activation by EBNA3C was impaired. This overturns previous assumptions about BMI1/PRC1 functions during EBNA3C-mediated regulation, for the first time identifies directly a host factor involved in EBNA3-mediated activation and provides a new insight into how PRC1 can be involved in gene activation.
AU  - Farrell,P
AU  - Paschos,K
DO  - nar/gky1323
EP  - 2821
PY  - 2019///
SN  - 0305-1048
SP  - 2807
TI  - Requirement for PRC1 subunit BMI1 in host gene activation by Epstein-Barr virus potein EBNA3C
T2  - Nucleic Acids Research
UR  - http://dx.doi.org/10.1093/nar/gky1323
UR  - http://hdl.handle.net/10044/1/66917
VL  - 47
ER  -
Download