Journal
MOLECULAR CELL
Volume 77, Issue 3, Pages 475-+Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2019.10.020
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Funding
- Spanish Ministry of Economy and Competitiveness Centro de Excelencia Severo Ochoa 2013-2017 [SEV-2012-0208, BFU2016-76141-P]
- ACER
- Italian Association for Cancer Research (AIRC) [IG16877]
- Cancer Research UK Programme Foundation [CR-UK C47547/A21536]
- Wellcome Trust Investigator Award [200818/Z/16/Z]
- European Research Council (ERC) under the European Union [609989-4DGenome]
- Spanish Ministry of Science, Innovation, and Universities
- CERCA Programme/Generalitat de Catalunya
- Centro de Excelencia Severo Ochoa
- ERC
- Ligue Contre le Cancer
- ISCIII [PT17/0019]
- ERDF [PT17/0019]
- Wellcome Trust [200818/Z/16/Z] Funding Source: Wellcome Trust
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How repetitive elements, epigenetic modifications, and architectural proteins interact ensuring proper genome expression remains poorly understood. Here, we report regulatory mechanisms unveiling a central role of Alu elements (AEs) and RNA polymerase III transcription factor C (TFIIIC) in structurally and functionally modulating the genome via chromatin looping and histone acetylation. Upon serum deprivation, a subset of AEs pre-marked by the activity-dependent neuroprotector homeobox Protein (ADNP) and located near cell-cycle genes recruits TFIIIC, which alters their chromatin accessibility by direct acetylation of histone H3 lysine-18 (H3K18). This facilitates the contacts of AEs with distant CTCF sites near promoter of other cell-cycle genes, which also become hyperacetylated at H3K18. These changes ensure basal transcription of cell-cycle genes and are critical for their re-activation upon serum re-exposure. Our study reveals how direct manipulation of the epigenetic state of AEs by a general transcription factor regulates 3D genome folding and expression.
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