Viral retasking of hBre1/RNF20 to recruit hPaf1 for transcriptional activation.

Upon infection, human adenovirus (HAdV) must activate the expression of its early genes to reprogram the cellular environment to support virus replication. This activation is orchestrated in large part by the first HAdV gene expressed during infection, early region 1A (E1A). E1A binds and appropriat...

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Autores principales:	Gregory J Fonseca, Michael J Cohen, Anthony C Nichols, John W Barrett, Joe S Mymryk
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/0f95c95895334819a3086eb8c23e9d38
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spelling	oai:doaj.org-article:0f95c95895334819a3086eb8c23e9d382021-11-18T06:05:32ZViral retasking of hBre1/RNF20 to recruit hPaf1 for transcriptional activation.1553-73661553-737410.1371/journal.ppat.1003411https://doaj.org/article/0f95c95895334819a3086eb8c23e9d382013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23785282/pdf/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Upon infection, human adenovirus (HAdV) must activate the expression of its early genes to reprogram the cellular environment to support virus replication. This activation is orchestrated in large part by the first HAdV gene expressed during infection, early region 1A (E1A). E1A binds and appropriates components of the cellular transcriptional machinery to modulate cellular gene transcription and activate viral early genes transcription. Previously, we identified hBre1/RNF20 as a target for E1A. The interaction between E1A and hBre1 antagonizes the innate antiviral response by blocking H2B monoubiquitination, a chromatin modification necessary for the interferon (IFN) response. Here, we describe a second distinct role for the interaction of E1A with hBre1 in transcriptional activation of HAdV early genes. Furthermore, we show that E1A changes the function of hBre1 from a ubiquitin ligase involved in substrate selection to a scaffold which recruits hPaf1 as a means to stimulate transcription and transcription-coupled histone modifications. By using hBre1 to recruit hPaf1, E1A is able to optimally activate viral early transcription and begin the cycle of viral replication. The ability of E1A to target hBre1 to simultaneously repress cellular IFN dependent transcription while activating viral transcription, represents an elegant example of the incredible economy of action accomplished by a viral regulatory protein through a single protein interaction.Gregory J FonsecaMichael J CohenAnthony C NicholsJohn W BarrettJoe S MymrykPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 9, Iss 6, p e1003411 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Gregory J Fonseca Michael J Cohen Anthony C Nichols John W Barrett Joe S Mymryk Viral retasking of hBre1/RNF20 to recruit hPaf1 for transcriptional activation.
description	Upon infection, human adenovirus (HAdV) must activate the expression of its early genes to reprogram the cellular environment to support virus replication. This activation is orchestrated in large part by the first HAdV gene expressed during infection, early region 1A (E1A). E1A binds and appropriates components of the cellular transcriptional machinery to modulate cellular gene transcription and activate viral early genes transcription. Previously, we identified hBre1/RNF20 as a target for E1A. The interaction between E1A and hBre1 antagonizes the innate antiviral response by blocking H2B monoubiquitination, a chromatin modification necessary for the interferon (IFN) response. Here, we describe a second distinct role for the interaction of E1A with hBre1 in transcriptional activation of HAdV early genes. Furthermore, we show that E1A changes the function of hBre1 from a ubiquitin ligase involved in substrate selection to a scaffold which recruits hPaf1 as a means to stimulate transcription and transcription-coupled histone modifications. By using hBre1 to recruit hPaf1, E1A is able to optimally activate viral early transcription and begin the cycle of viral replication. The ability of E1A to target hBre1 to simultaneously repress cellular IFN dependent transcription while activating viral transcription, represents an elegant example of the incredible economy of action accomplished by a viral regulatory protein through a single protein interaction.
format	article
author	Gregory J Fonseca Michael J Cohen Anthony C Nichols John W Barrett Joe S Mymryk
author_facet	Gregory J Fonseca Michael J Cohen Anthony C Nichols John W Barrett Joe S Mymryk
author_sort	Gregory J Fonseca
title	Viral retasking of hBre1/RNF20 to recruit hPaf1 for transcriptional activation.
title_short	Viral retasking of hBre1/RNF20 to recruit hPaf1 for transcriptional activation.
title_full	Viral retasking of hBre1/RNF20 to recruit hPaf1 for transcriptional activation.
title_fullStr	Viral retasking of hBre1/RNF20 to recruit hPaf1 for transcriptional activation.
title_full_unstemmed	Viral retasking of hBre1/RNF20 to recruit hPaf1 for transcriptional activation.
title_sort	viral retasking of hbre1/rnf20 to recruit hpaf1 for transcriptional activation.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/0f95c95895334819a3086eb8c23e9d38
work_keys_str_mv	AT gregoryjfonseca viralretaskingofhbre1rnf20torecruithpaf1fortranscriptionalactivation AT michaeljcohen viralretaskingofhbre1rnf20torecruithpaf1fortranscriptionalactivation AT anthonycnichols viralretaskingofhbre1rnf20torecruithpaf1fortranscriptionalactivation AT johnwbarrett viralretaskingofhbre1rnf20torecruithpaf1fortranscriptionalactivation AT joesmymryk viralretaskingofhbre1rnf20torecruithpaf1fortranscriptionalactivation
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Viral retasking of hBre1/RNF20 to recruit hPaf1 for transcriptional activation.

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