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Alex Meltzer 1,†, Aditi Gupta 1,†, Phyo Nay Lin 1, Robert A. Brown 1, Daniel S. Benyamien-Roufaeil 1, Raju Khatri 1, Anup A. Mahurkar 2, Yang Song 2, Rodney J. Taylor 3,4 and Michal Zalzman 1,3,4,5, *  \nCitation: Meltzer, W.A.; Gupta, A.; Lin, P.N.; Brown, R.A.;  \nBenyamien-Roufaeil, D.S.; Khatri, R.; Mahurkar, A.A.; Song, Y.; Taylor, R.J.; Zalzman, M. Reprogramming Chromosome Ends by Functional Histone Acetylation. Int. J. Mol. Sci. 2024, 25, 3898. [https://doi.org/](https://doi.org/)[ ](https://doi.org/)[10.3390/ijms25073898](10.3390/ijms25073898)  \nAcademic Editor: Alla Kalmykova  \nReceived: 30 January 2024  \nRevised: 26 March 2024  \nAccepted: 28 March 2024  \nPublished: 31 March 2024  \nCopyright: © 2024 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://](https://)[ ](https://)[creativecommons.org/licenses/by/](creativecommons.org/licenses/by/)[ ](creativecommons.org/licenses/by/)[4.0/](4.0/)) .  \n1 Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD 21201, USA; [aditi.gupta@nih.gov](aditi.gupta@nih.gov) (A.G.); [phyonaylinn@gmail.com](phyonaylinn@gmail.com) (P.N.L.); [rabrown@som.umaryland.edu](rabrown@som.umaryland.edu) (R.A.B.); [dbenyamienroufaeil@som.umaryland.edu](dbenyamienroufaeil@som.umaryland.edu) (D.S.B.-R.); [ghiraju@gmail.com](ghiraju@gmail.com) (R.K.)  \n2 Institute for Genome Sciences, University of Maryland School of Medicine, Baltimore, MD 21201, USA; [amahurkar@som.umaryland.edu](amahurkar@som.umaryland.edu) (A.A.M.); [ysong@som.umaryland.edu](ysong@som.umaryland.edu) (Y.S.)  \n3 Department of Otorhinolaryngology-Head and Neck Surgery, University of Maryland School of Medicine, Baltimore, MD 21201, USA; [rtaylor@som.umaryland.edu](rtaylor@som.umaryland.edu)  \n4 Marlene and Stewart Greenbaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD 21201, USA  \n5 The Center for Stem Cell Biology and Regenerative Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA  \n* [Correspondence: mzalzman@som.umaryland.edu](Correspondence: mzalzman@som.umaryland.edu); Tel.: +1-410-706-7879 † These authors contributed equally to this work.  \nAbstract: Cancers harness embryonic programs to evade aging and promote survival. Normally, sequences at chromosome ends called telomeres shorten with cell division, serving as a countdown clock to limit cell replication. Therefore, a crucial aspect of cancerous transformation is avoiding replicative aging by activation of telomere repair programs. Mouse embryonic stem cells (mESCs) activate a transient expression of the gene Zscan4, which correlates with chromatin de-condensation and telomere extension. Head and neck squamous cell carcinoma (HNSCC) cancers reactivate ZSCAN4, which in turn regulates the phenotype of cancer stem cells (CSCs) . Our study reveals a new role for human ZSCAN4 in facilitating functional histone H3 acetylation at telomere chromatin. Nextgeneration sequencing indicates ZSCAN4 enrichment at telomere chromatin. These changes correlate with ZSCAN4-induced histone H3 acetylation and telomere elongation, while CRISPR/Cas9 knockout of ZSCAN4 leads to reduced H3 acetylation and telomere shortening. Our study elucidates the intricate involvement of ZSCAN4 and its significant contribution to telomere chromatin remodeling. These findings suggest that ZSCAN4 induction serves as a novel link between ‘stemness’ and telomere maintenance. Targeting ZSCAN4 may offer new therapeutic approaches to effectively limit or enhance the replicative lifespan of stem cells and cancer cells.  \nKeywords: telomeres; ZSCAN4; epigenetics; histone acetylation; pluripotency; stem cells; cancer; CRISPR; over-expression; next-gen sequencing  \n1. Introduction  \nTelomeres are repetitiv","cbCaicpxZ0nqmO8h","https://ap.wps.com/l/cbCaicpxZ0nqmO8h","pdf",3508531,15,"English","# Introduction\n## Telomere shortening and replication limits\n## Telomere maintenance and chromatin accessibility\n## ZSCAN4 in embryonic stem cells and genome stability\n## ZSCAN4 links to chromatin remodeling","[{\"question\":\"What problem does the study address regarding cancer and aging?\",\"answer\":\"Cancer cells evade replicative aging by activating telomere repair programs that prevent telomere shortening during division.\"},{\"question\":\"What does ZSCAN4 do at telomere chromatin in this study?\",\"answer\":\"ZSCAN4 facilitates functional histone H3 acetylation at telomere chromatin and correlates with telomere elongation.\"},{\"question\":\"How were ZSCAN4’s effects tested experimentally?\",\"answer\":\"The study used next-generation sequencing to assess ZSCAN4 enrichment at telomeres and CRISPR/Cas9 knockout to measure changes in H3 acetylation and telomere length.\"}]","Reprogramming Chromosome Ends by Functional Histone Acetylation | PDF",1789988874,38]