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One of the main causes of neurodegeneration in HD is transcriptional dysregulation that, in part, is caused by the inhibition of histone acetyltransferase (HAT) enzymes. HD pathology can be alleviated by increasing the activity of specific HATs or by inhibiting histone deacetylase (HDAC) enzymes. To determine which histone\u2019s post-translational modifications (PTMs) might play crucial roles in HD pathology, we investigated the phenotype-modifying effects of PTM mimetic mutations of variant histone H3.3 in a Drosophila model of HD. Specifically, we studied the mutations (K\u2192Q: acetylated; K\u2192R: non-modified; and K\u2192M: methylated) of lysine residues K9, K14, and K27 of transgenic H3.3. In the case of H3.3K14Q modification, we observed the amelioration of all tested phenotypes (viability, longevity, neurodegeneration, motor activity, and circadian rhythm defects), while H3.3K14R had the opposite effect. H3.3K14Q expression prevented the negative effects of reduced Gcn5 (a HAT acting on H3K14) on HD pathology, while it only partially hindered the positive effects of heterozygous Sirt1 (an HDAC acting on H3K14). Thus, we conclude that the Gcn5-dependent acetylation of H3.3K14 might be an important epigenetic contributor to HD pathology.<\/jats:p>","DOI":"10.3390\/ijms232315173","type":"journal-article","created":{"date-parts":[[2022,12,5]],"date-time":"2022-12-05T01:42:21Z","timestamp":1670204541000},"page":"15173","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Acetylation State of Lysine 14 of Histone H3.3 Affects Mutant Huntingtin Induced Pathogenesis"],"prefix":"10.3390","volume":"23","author":[{"given":"Anik\u00f3","family":"Farag\u00f3","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Faculty of Science and Informatics, University of Szeged, K\u00f6z\u00e9p fasor 52, H-6726 Szeged, Hungary"},{"name":"Doctoral School in Biology, Faculty of Science and Informatics, University of Szeged, H-6726 Szeged, Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6189-3100","authenticated-orcid":false,"given":"N\u00f3ra","family":"Zsindely","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Faculty of Science and Informatics, University of Szeged, K\u00f6z\u00e9p fasor 52, H-6726 Szeged, Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anita","family":"Farkas","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Faculty of Science and Informatics, University of Szeged, K\u00f6z\u00e9p fasor 52, H-6726 Szeged, Hungary"},{"name":"Doctoral School in Biology, Faculty of Science and Informatics, University of Szeged, H-6726 Szeged, Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alexandra","family":"Neller","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Faculty of Science and Informatics, University of Szeged, K\u00f6z\u00e9p fasor 52, H-6726 Szeged, Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fruzsina","family":"Si\u00e1gi","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Faculty of Science and Informatics, University of Szeged, K\u00f6z\u00e9p fasor 52, H-6726 Szeged, Hungary"},{"name":"Doctoral School in Biology, Faculty of Science and Informatics, University of Szeged, H-6726 Szeged, Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0415-5192","authenticated-orcid":false,"given":"M\u00e1rton Rich\u00e1rd","family":"Szab\u00f3","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Albert Szent-Gy\u00f6rgyi Medical School, University of Szeged, H-6720 Szeged, Hungary"},{"name":"Interdisciplinary Centre of Excellence, University of Szeged, H-6720 Szeged, Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tam\u00e1s","family":"Csont","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Albert Szent-Gy\u00f6rgyi Medical School, University of Szeged, H-6720 Szeged, Hungary"},{"name":"Interdisciplinary Centre of Excellence, University of Szeged, H-6720 Szeged, Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8411-626X","authenticated-orcid":false,"given":"L\u00e1szl\u00f3","family":"Bodai","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Faculty of Science and Informatics, University of Szeged, K\u00f6z\u00e9p fasor 52, H-6726 Szeged, Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2022,12,2]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"15005","DOI":"10.1038\/nrdp.2015.5","article-title":"Huntington Disease","volume":"1","author":"Bates","year":"2015","journal-title":"Nat. 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