Reference : The varicella-zoster virus immediate-early 63 protein affects chromatin-controlled gene ...
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
http://hdl.handle.net/2268/1114
The varicella-zoster virus immediate-early 63 protein affects chromatin-controlled gene transcription in a cell-type dependent manner.
English
Habran, Lionel mailto [Université de Liège - ULG > Sciences de la Vie > GIGA Research Virologie -Immunologie > > >]
El Mjiyad, Nadia mailto [Université de Liège > Département des sciences de la vie > Virologie - Immunologie GIGA-Research > >]
Di Valentin, Emmanuel mailto [Université de Liège > Département des sciences de la vie > Virologie - Immunologie GIGA-Research > >]
Sadzot-Delvaux, Catherine mailto [Université de Liège > Département des sciences de la vie > Virologie et immunologie - GIGA-Research > >]
Bontems, Sébastien mailto [Université de Liège > Sciences de la Vie > GIGA-Research Virologie - Immunologie > >]
Piette, Jacques mailto [Université de Liège > Département des sciences de la vie > Virologie - Immunologie - GIGA-Research >]
Oct-2007
BMC Molecular Biology
BioMed Central
8
99
Yes (verified by ORBi)
International
1471-2199
[en] Varicella zoster virus ; NF-KB
[en] Varicella Zoster Virus Immediate Early 63 protein (IE63) has been shown to be essential for VZV replication, and critical for latency establishment. The activity of the protein as a transcriptional regulator is not fully clear yet. Using transient transfection assays, IE63 has been shown to repress viral and cellular promoters containing typical TATA boxes by interacting with general transcription factors.
In this paper, IE63 regulation properties on endogenous gene expression were evaluated using an oligonucleotide-based micro-array approach. We found that IE63 modulates the transcription of only a few genes in HeLa cells including genes implicated in transcription or immunity. Furthermore, we showed that this effect is mediated by a modification of RNA POL II binding on the promoters tested and that IE63 phosphorylation was essential for these effects. In MeWo cells, the number of genes whose transcription was modified by IE63 was somewhat higher, including genes implicated in signal transduction, transcription, immunity, and heat-shock signalling. While IE63 did not modify the basal expression of several NF-κB dependent genes such as IL-8, ICAM-1, and IκBα, it modulates transcription of these genes upon TNFα induction. This effect was obviously correlated with the amount of p65 binding to the promoter of these genes and with histone H3 acetylation and HDAC-3 removal.
Conclusion
While IE63 only affected transcription of a small number of cellular genes, it interfered with the TNF-inducibility of several NF-κB dependent genes by the accelerated resynthesis of the inhibitor IκBα.
Giga-Infection, Immunity and Inflammation
Fonds de la Recherche Scientifique (Communauté française de Belgique) - F.R.S.-FNRS
Researchers
http://hdl.handle.net/2268/1114
10.1186/1471-2199-8-99
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17971236

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