TFIIIC as a potential epigenetic modulator of histone acetylation in human stem cells

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• dc.contributor.author Vezzoli, Marco
• dc.contributor.author De Llobet, Lara Isabel
• dc.contributor.author Di Vona, Chiara, 1981-
• dc.contributor.author Morselli, Marco
• dc.contributor.author Montanini, Barbara
• dc.contributor.author Luna Gargantilla, Susana de la
• dc.contributor.author Teichmann, Martin
• dc.contributor.author Dieci, Giorgio
• dc.contributor.author Ferrari, Roberto
• dc.date.accessioned 2023-06-08T06:49:01Z
• dc.date.available 2023-06-08T06:49:01Z
• dc.date.issued 2023
• dc.description.abstract Regulation of histone acetylation dictates patterns of gene expression and hence cell identity. Due to their clinical relevance in cancer biology, understanding how human embryonic stem cells (hESCs) regulate their genomic patterns of histone acetylation is critical, but it remains largely to be investigated. Here, we provide evidence that acetylation of histone H3 lysine-18 (H3K18ac) and lysine-27 (H3K27ac) is only partially established by p300 in stem cells, while it represents the main histone acetyltransferase (HAT) for these marks in somatic cells. Our analysis reveals that whereas p300 marginally associated with H3K18ac and H3K27ac in hESCs, it largely overlapped with these histone marks upon differentiation. Interestingly, we show that H3K18ac is found at "stemness" genes enriched in RNA polymerase III transcription factor C (TFIIIC) in hESCs, whilst lacking p300. Moreover, TFIIIC was also found in the vicinity of genes involved in neuronal biology, although devoid of H3K18ac. Our data suggest a more complex pattern of HATs responsible for histone acetylations in hESCs than previously considered, suggesting a putative role for H3K18ac and TFIIIC in regulating "stemness" genes as well as genes associated with neuronal differentiation of hESCs. The results break ground for possible new paradigms for genome acetylation in hESCs that could lead to new avenues for therapeutic intervention in cancer and developmental diseases.
• dc.description.sponsorship This work was supported by Bando Galileo 2022 (G22-142) to R.F. and M.T. The research is also supported by the AIRC IG Grant 27712-A to R.F. This work was also supported by the Spanish Ministry of Science and Innovation (PID2019-107185GB-I00) to S.d.l.L. The CRG acknowledge the support of the Spanish Ministry of Science and Innovation to the EMBL partnership, the Centro de Excelencia Severo Ochoa and the support of the CERCA Programme/Generalitat de Catalunya. This work was also supported by the Ligue Contre le Cancer, committees des Landes et de la Dordogne to M.T.
• dc.format.mimetype application/pdf
• dc.identifier.citation Vezzoli M, de Llobet Cucalon LI, Di Vona C, Morselli M, Montanini B, de la Luna S, et al. TFIIIC as a potential epigenetic modulator of histone acetylation in human stem cells. IJMS. 2023 Feb 2;24(4):3624. DOI: 10.3390/ijms24043624
• dc.identifier.doi http://dx.doi.org/10.3390/ijms24043624
• dc.identifier.issn 1661-6596
• dc.identifier.uri http://hdl.handle.net/10230/57112
• dc.language.iso eng
• dc.publisher MDPI
• dc.relation.ispartof IJMS. 2023 Feb 2;24(4):3624
• dc.relation.projectID info:eu-repo/grantAgreement/ES/2PE/PID2019-107185GB-I00
• dc.rights © 2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
• dc.rights.accessRights info:eu-repo/semantics/openAccess
• dc.rights.uri http://creativecommons.org/licenses/by/4.0/
• dc.subject.keyword H3K18ac
• dc.subject.keyword H3K27ac
• dc.subject.keyword TFIIIC
• dc.subject.keyword Acetylation
• dc.subject.keyword hESCs
• dc.subject.keyword Neurogenesis
• dc.subject.keyword p300
• dc.title TFIIIC as a potential epigenetic modulator of histone acetylation in human stem cells
• dc.type info:eu-repo/semantics/article
• dc.type.version info:eu-repo/semantics/publishedVersion