The regulation of DNA end resection by chromatin response to DNA double strand breaks
DNA double-strand breaks (DSBs) constantly arise upon exposure to genotoxic agents and during physiological processes. The timely repair of DSBs is important for not only the completion of the cellular functions involving DSBs as intermediates, but also the maintenance of genome stability. There are...
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Format: | Article |
Language: | English |
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Frontiers Media S.A.
2022-07-01
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Series: | Frontiers in Cell and Developmental Biology |
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Online Access: | https://www.frontiersin.org/articles/10.3389/fcell.2022.932633/full |
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author | Bo-Ruei Chen Bo-Ruei Chen Barry P. Sleckman Barry P. Sleckman |
author_facet | Bo-Ruei Chen Bo-Ruei Chen Barry P. Sleckman Barry P. Sleckman |
author_sort | Bo-Ruei Chen |
collection | DOAJ |
description | DNA double-strand breaks (DSBs) constantly arise upon exposure to genotoxic agents and during physiological processes. The timely repair of DSBs is important for not only the completion of the cellular functions involving DSBs as intermediates, but also the maintenance of genome stability. There are two major pathways dedicated to DSB repair: homologous recombination (HR) and non-homologous end joining (NHEJ). The decision of deploying HR or NHEJ to repair DSBs largely depends on the structures of broken DNA ends. DNA ends resected to generate extensive single-strand DNA (ssDNA) overhangs are repaired by HR, while those remaining blunt or minimally processed can be repaired by NHEJ. As the generation and repair of DSB occurs within the context of chromatin, the resection of broken DNA ends is also profoundly affected by the state of chromatin flanking DSBs. Here we review how DNA end resection can be regulated by histone modifications, chromatin remodeling, and the presence of ssDNA structure through altering the accessibility to chromatin and the activity of pro- and anti-resection proteins. |
first_indexed | 2024-12-11T02:32:21Z |
format | Article |
id | doaj.art-89465caba2e44955b228127e728e3ad5 |
institution | Directory Open Access Journal |
issn | 2296-634X |
language | English |
last_indexed | 2024-12-11T02:32:21Z |
publishDate | 2022-07-01 |
publisher | Frontiers Media S.A. |
record_format | Article |
series | Frontiers in Cell and Developmental Biology |
spelling | doaj.art-89465caba2e44955b228127e728e3ad52022-12-22T01:23:49ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2022-07-011010.3389/fcell.2022.932633932633The regulation of DNA end resection by chromatin response to DNA double strand breaksBo-Ruei Chen0Bo-Ruei Chen1Barry P. Sleckman2Barry P. Sleckman3Division of Hematology and Oncology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, United StatesO’Neal Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, United StatesDivision of Hematology and Oncology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, United StatesO’Neal Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, United StatesDNA double-strand breaks (DSBs) constantly arise upon exposure to genotoxic agents and during physiological processes. The timely repair of DSBs is important for not only the completion of the cellular functions involving DSBs as intermediates, but also the maintenance of genome stability. There are two major pathways dedicated to DSB repair: homologous recombination (HR) and non-homologous end joining (NHEJ). The decision of deploying HR or NHEJ to repair DSBs largely depends on the structures of broken DNA ends. DNA ends resected to generate extensive single-strand DNA (ssDNA) overhangs are repaired by HR, while those remaining blunt or minimally processed can be repaired by NHEJ. As the generation and repair of DSB occurs within the context of chromatin, the resection of broken DNA ends is also profoundly affected by the state of chromatin flanking DSBs. Here we review how DNA end resection can be regulated by histone modifications, chromatin remodeling, and the presence of ssDNA structure through altering the accessibility to chromatin and the activity of pro- and anti-resection proteins.https://www.frontiersin.org/articles/10.3389/fcell.2022.932633/fullDNA end resectionhomologous recombinationnon-homologous end joininghistone modificaitonschromatin remodeling53BP1 |
spellingShingle | Bo-Ruei Chen Bo-Ruei Chen Barry P. Sleckman Barry P. Sleckman The regulation of DNA end resection by chromatin response to DNA double strand breaks Frontiers in Cell and Developmental Biology DNA end resection homologous recombination non-homologous end joining histone modificaitons chromatin remodeling 53BP1 |
title | The regulation of DNA end resection by chromatin response to DNA double strand breaks |
title_full | The regulation of DNA end resection by chromatin response to DNA double strand breaks |
title_fullStr | The regulation of DNA end resection by chromatin response to DNA double strand breaks |
title_full_unstemmed | The regulation of DNA end resection by chromatin response to DNA double strand breaks |
title_short | The regulation of DNA end resection by chromatin response to DNA double strand breaks |
title_sort | regulation of dna end resection by chromatin response to dna double strand breaks |
topic | DNA end resection homologous recombination non-homologous end joining histone modificaitons chromatin remodeling 53BP1 |
url | https://www.frontiersin.org/articles/10.3389/fcell.2022.932633/full |
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