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Chromatin structure and DNA damage repair

The integrity of the genome is continuously challenged by both endogenous and exogenous DNA damaging agents. These damaging agents can induce a wide variety of lesions in the DNA, such as double strand breaks, single strand breaks, oxidative lesions and pyrimidine dimers. The cell has evolved intric...

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Detalles Bibliográficos
Autores principales: Dinant, Christoffel, Houtsmuller, Adriaan B, Vermeulen, Wim
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2596136/
https://www.ncbi.nlm.nih.gov/pubmed/19014481
http://dx.doi.org/10.1186/1756-8935-1-9
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author Dinant, Christoffel
Houtsmuller, Adriaan B
Vermeulen, Wim
author_facet Dinant, Christoffel
Houtsmuller, Adriaan B
Vermeulen, Wim
author_sort Dinant, Christoffel
collection PubMed
description The integrity of the genome is continuously challenged by both endogenous and exogenous DNA damaging agents. These damaging agents can induce a wide variety of lesions in the DNA, such as double strand breaks, single strand breaks, oxidative lesions and pyrimidine dimers. The cell has evolved intricate DNA damage response mechanisms to counteract the genotoxic effects of these lesions. The two main features of the DNA damage response mechanisms are cell-cycle checkpoint activation and, at the heart of the response, DNA repair. For both damage signalling and repair, chromatin remodelling is most likely a prerequisite. Here, we discuss current knowledge on chromatin remodelling with respect to the cellular response to DNA damage, with emphasis on the response to lesions resolved by nucleotide excision repair. We will discuss the role of histone modifications as well as their displacement or exchange in nucleotide excision repair and make a comparison with their requirement in transcription and double strand break repair.
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spelling pubmed-25961362008-12-05 Chromatin structure and DNA damage repair Dinant, Christoffel Houtsmuller, Adriaan B Vermeulen, Wim Epigenetics Chromatin Review The integrity of the genome is continuously challenged by both endogenous and exogenous DNA damaging agents. These damaging agents can induce a wide variety of lesions in the DNA, such as double strand breaks, single strand breaks, oxidative lesions and pyrimidine dimers. The cell has evolved intricate DNA damage response mechanisms to counteract the genotoxic effects of these lesions. The two main features of the DNA damage response mechanisms are cell-cycle checkpoint activation and, at the heart of the response, DNA repair. For both damage signalling and repair, chromatin remodelling is most likely a prerequisite. Here, we discuss current knowledge on chromatin remodelling with respect to the cellular response to DNA damage, with emphasis on the response to lesions resolved by nucleotide excision repair. We will discuss the role of histone modifications as well as their displacement or exchange in nucleotide excision repair and make a comparison with their requirement in transcription and double strand break repair. BioMed Central 2008-11-12 /pmc/articles/PMC2596136/ /pubmed/19014481 http://dx.doi.org/10.1186/1756-8935-1-9 Text en Copyright © 2008 Dinant et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Dinant, Christoffel
Houtsmuller, Adriaan B
Vermeulen, Wim
Chromatin structure and DNA damage repair
title Chromatin structure and DNA damage repair
title_full Chromatin structure and DNA damage repair
title_fullStr Chromatin structure and DNA damage repair
title_full_unstemmed Chromatin structure and DNA damage repair
title_short Chromatin structure and DNA damage repair
title_sort chromatin structure and dna damage repair
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2596136/
https://www.ncbi.nlm.nih.gov/pubmed/19014481
http://dx.doi.org/10.1186/1756-8935-1-9
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