Association of the interferon-β gene with pericentromeric heterochromatin is dynamically regulated during virus infection through a YY1-dependent mechanism

Nuclear architecture as well as gene nuclear positioning can modulate gene expression. In this work, we have analyzed the nuclear position of the interferon-β (IFN-β) locus, responsible for the establishment of the innate antiviral response, with respect to pericentromeric heterochromatin (PCH) in c...

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Bibliographic Details
Published in:	Nucleic acids research Vol. 40; no. 10; pp. 4396 - 4411
Main Authors:	Josse, T, Mokrani-Benhelli, H, Benferhat, R, Shestakova, E, Mansuroglu, Z, Kakanakou, H, Billecocq, A, Bouloy, M, Bonnefoy, Eliette
Format:	Journal Article
Language:	English
Published:	England Oxford University Press 01-05-2012
Subjects:	Animals beta -Interferon Binding Sites Cell Line DNA, Satellite - analysis Gene expression Gene Regulation, Chromatin and Epigenetics Heterochromatin Heterochromatin - chemistry Infection Interferon-beta - genetics Mice Newcastle disease virus - physiology Promoter Regions, Genetic Promoters Rift Valley fever virus - physiology Transcription activation Transcriptional Activation YY1 Transcription Factor - metabolism
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Summary:	Nuclear architecture as well as gene nuclear positioning can modulate gene expression. In this work, we have analyzed the nuclear position of the interferon-β (IFN-β) locus, responsible for the establishment of the innate antiviral response, with respect to pericentromeric heterochromatin (PCH) in correlation with virus-induced IFN-β gene expression. Experiments were carried out in two different cell types either non-infected (NI) or during the time course of three different viral infections. In NI cells, we showed a monoallelic IFN-β promoter association with PCH that strongly decreased after viral infection. Dissociation of the IFN-β locus away from these repressive regions preceded strong promoter transcriptional activation and was reversible within 12 h after infection. No dissociation was observed after infection with a virus that abnormally maintained the IFN-β gene in a repressed state. Dissociation induced after virus infection specifically targeted the IFN-β locus without affecting the general structure and nuclear distribution of PCH clusters. Using cell lines stably transfected with wild-type or mutated IFN-β promoters, we identified the proximal region of the IFN-β promoter containing YY1 DNA-binding sites as the region regulating IFN-β promoter association with PCH before as well as during virus infection.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors. Present address: E. Shestakova, Centre de Recherche, Hopital Maisonneuve-Rosemont, 5415 boul. de l'Assomption, Montreal, Quebec, H1T 2M4, Canada.
ISSN:	0305-1048 1362-4962
DOI:	10.1093/nar/gks050