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The Sound of Silence: How Silenced Chromatin Orchestrates the Repair of Double-Strand Breaks

The eukaryotic nucleus is continuously being exposed to endogenous and exogenous sources that cause DNA breaks, whose faithful repair requires the activity of dedicated nuclear machineries. DNA is packaged into a variety of chromatin domains, each characterized by specific molecular properties that...

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Detalles Bibliográficos
Autores principales: Kendek, Apfrida, Wensveen, Marieke R., Janssen, Aniek
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8467445/
https://www.ncbi.nlm.nih.gov/pubmed/34573397
http://dx.doi.org/10.3390/genes12091415
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author Kendek, Apfrida
Wensveen, Marieke R.
Janssen, Aniek
author_facet Kendek, Apfrida
Wensveen, Marieke R.
Janssen, Aniek
author_sort Kendek, Apfrida
collection PubMed
description The eukaryotic nucleus is continuously being exposed to endogenous and exogenous sources that cause DNA breaks, whose faithful repair requires the activity of dedicated nuclear machineries. DNA is packaged into a variety of chromatin domains, each characterized by specific molecular properties that regulate gene expression and help maintain nuclear structure. These different chromatin environments each demand a tailored response to DNA damage. Silenced chromatin domains in particular present a major challenge to the cell’s DNA repair machinery due to their specific biophysical properties and distinct, often repetitive, DNA content. To this end, we here discuss the interplay between silenced chromatin domains and DNA damage repair, specifically double-strand breaks, and how these processes help maintain genome stability.
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spelling pubmed-84674452021-09-27 The Sound of Silence: How Silenced Chromatin Orchestrates the Repair of Double-Strand Breaks Kendek, Apfrida Wensveen, Marieke R. Janssen, Aniek Genes (Basel) Review The eukaryotic nucleus is continuously being exposed to endogenous and exogenous sources that cause DNA breaks, whose faithful repair requires the activity of dedicated nuclear machineries. DNA is packaged into a variety of chromatin domains, each characterized by specific molecular properties that regulate gene expression and help maintain nuclear structure. These different chromatin environments each demand a tailored response to DNA damage. Silenced chromatin domains in particular present a major challenge to the cell’s DNA repair machinery due to their specific biophysical properties and distinct, often repetitive, DNA content. To this end, we here discuss the interplay between silenced chromatin domains and DNA damage repair, specifically double-strand breaks, and how these processes help maintain genome stability. MDPI 2021-09-15 /pmc/articles/PMC8467445/ /pubmed/34573397 http://dx.doi.org/10.3390/genes12091415 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/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/).
spellingShingle Review
Kendek, Apfrida
Wensveen, Marieke R.
Janssen, Aniek
The Sound of Silence: How Silenced Chromatin Orchestrates the Repair of Double-Strand Breaks
title The Sound of Silence: How Silenced Chromatin Orchestrates the Repair of Double-Strand Breaks
title_full The Sound of Silence: How Silenced Chromatin Orchestrates the Repair of Double-Strand Breaks
title_fullStr The Sound of Silence: How Silenced Chromatin Orchestrates the Repair of Double-Strand Breaks
title_full_unstemmed The Sound of Silence: How Silenced Chromatin Orchestrates the Repair of Double-Strand Breaks
title_short The Sound of Silence: How Silenced Chromatin Orchestrates the Repair of Double-Strand Breaks
title_sort sound of silence: how silenced chromatin orchestrates the repair of double-strand breaks
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8467445/
https://www.ncbi.nlm.nih.gov/pubmed/34573397
http://dx.doi.org/10.3390/genes12091415
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