Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1-bound enhancers through interactions with the EP400 chromatin remodeler.

Autor:	Cantarella S; Department of Chemistry, Life Sciences and Environmental Sustainability, University of Parma, 43124 Parma, Italy., Vezzoli M; Department of Chemistry, Life Sciences and Environmental Sustainability, University of Parma, 43124 Parma, Italy., Carnevali D; Department of Chemistry, Life Sciences and Environmental Sustainability, University of Parma, 43124 Parma, Italy., Morselli M; Department of Chemistry, Life Sciences and Environmental Sustainability, University of Parma, 43124 Parma, Italy., Zemke NR; Molecular Biology Institute, University of California at Los Angeles, Los Angeles, CA 90095, USA., Montanini B; Department of Chemistry, Life Sciences and Environmental Sustainability, University of Parma, 43124 Parma, Italy., Daussy CF; Bordeaux University, CNRS UMR 5234, Fundamental Microbiology and Pathogenicity, Bordeaux, France., Wodrich H; Bordeaux University, CNRS UMR 5234, Fundamental Microbiology and Pathogenicity, Bordeaux, France., Teichmann M; Bordeaux University, Inserm U 1312, Bordeaux Institute of Oncology, 33076 Bordeaux, France., Pellegrini M; Department of Molecular Cellular and Developmental Biology, University of California Los Angeles, Los Angeles, CA 90095, USA., Berk AJ; Molecular Biology Institute, University of California at Los Angeles, Los Angeles, CA 90095, USA., Dieci G; Department of Chemistry, Life Sciences and Environmental Sustainability, University of Parma, 43124 Parma, Italy., Ferrari R; Department of Chemistry, Life Sciences and Environmental Sustainability, University of Parma, 43124 Parma, Italy.
Jazyk:	angličtina
Zdroj:	Nucleic acids research [Nucleic Acids Res] 2024 Sep 09; Vol. 52 (16), pp. 9481-9500.
DOI:	10.1093/nar/gkae615
Abstrakt:	Alu retrotransposons, which form the largest family of mobile DNA elements in the human genome, have recently come to attention as a potential source of regulatory novelties, most notably by participating in enhancer function. Even though Alu transcription by RNA polymerase III is subjected to tight epigenetic silencing, their expression has long been known to increase in response to various types of stress, including viral infection. Here we show that, in primary human fibroblasts, adenovirus small e1a triggered derepression of hundreds of individual Alus by promoting TFIIIB recruitment by Alu-bound TFIIIC. Epigenome profiling revealed an e1a-induced decrease of H3K27 acetylation and increase of H3K4 monomethylation at derepressed Alus, making them resemble poised enhancers. The enhancer nature of e1a-targeted Alus was confirmed by the enrichment, in their upstream regions, of the EP300/CBP acetyltransferase, EP400 chromatin remodeler and YAP1 and FOS transcription factors. The physical interaction of e1a with EP400 was critical for Alu derepression, which was abrogated upon EP400 ablation. Our data suggest that e1a targets a subset of enhancer Alus whose transcriptional activation, which requires EP400 and is mediated by the e1a-EP400 interaction, may participate in the manipulation of enhancer activity by adenoviruses. (© The Author(s) 2024. Published by Oxford University Press on behalf of Nucleic Acids Research.)
Databáze:	MEDLINE
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