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Moving Mountains—The BRCA1 Promotion of DNA Resection

DNA double-strand breaks (DSBs) occur in our cells in the context of chromatin. This type of lesion is toxic, entirely preventing genome continuity and causing cell death or terminal arrest. Several repair mechanisms can act on DNA surrounding a DSB, only some of which carry a low risk of mutation,...

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Detalles Bibliográficos
Autores principales: Densham, Ruth M., Morris, Joanna R.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6733915/
https://www.ncbi.nlm.nih.gov/pubmed/31552267
http://dx.doi.org/10.3389/fmolb.2019.00079
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author Densham, Ruth M.
Morris, Joanna R.
author_facet Densham, Ruth M.
Morris, Joanna R.
author_sort Densham, Ruth M.
collection PubMed
description DNA double-strand breaks (DSBs) occur in our cells in the context of chromatin. This type of lesion is toxic, entirely preventing genome continuity and causing cell death or terminal arrest. Several repair mechanisms can act on DNA surrounding a DSB, only some of which carry a low risk of mutation, so that which repair process is utilized is critical to the stability of genetic material of cells. A key component of repair outcome is the degree of DNA resection directed to either side of the break site. This in turn determines the subsequent forms of repair in which DNA homology plays a part. Here we will focus on chromatin and chromatin-bound complexes which constitute the “mountains” that block resection, with a particular focus on how the breast and ovarian cancer predisposition protein-1 (BRCA1) contributes to repair outcomes through overcoming these blocks.
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spelling pubmed-67339152019-09-24 Moving Mountains—The BRCA1 Promotion of DNA Resection Densham, Ruth M. Morris, Joanna R. Front Mol Biosci Molecular Biosciences DNA double-strand breaks (DSBs) occur in our cells in the context of chromatin. This type of lesion is toxic, entirely preventing genome continuity and causing cell death or terminal arrest. Several repair mechanisms can act on DNA surrounding a DSB, only some of which carry a low risk of mutation, so that which repair process is utilized is critical to the stability of genetic material of cells. A key component of repair outcome is the degree of DNA resection directed to either side of the break site. This in turn determines the subsequent forms of repair in which DNA homology plays a part. Here we will focus on chromatin and chromatin-bound complexes which constitute the “mountains” that block resection, with a particular focus on how the breast and ovarian cancer predisposition protein-1 (BRCA1) contributes to repair outcomes through overcoming these blocks. Frontiers Media S.A. 2019-09-03 /pmc/articles/PMC6733915/ /pubmed/31552267 http://dx.doi.org/10.3389/fmolb.2019.00079 Text en Copyright © 2019 Densham and Morris. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Molecular Biosciences
Densham, Ruth M.
Morris, Joanna R.
Moving Mountains—The BRCA1 Promotion of DNA Resection
title Moving Mountains—The BRCA1 Promotion of DNA Resection
title_full Moving Mountains—The BRCA1 Promotion of DNA Resection
title_fullStr Moving Mountains—The BRCA1 Promotion of DNA Resection
title_full_unstemmed Moving Mountains—The BRCA1 Promotion of DNA Resection
title_short Moving Mountains—The BRCA1 Promotion of DNA Resection
title_sort moving mountains—the brca1 promotion of dna resection
topic Molecular Biosciences
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6733915/
https://www.ncbi.nlm.nih.gov/pubmed/31552267
http://dx.doi.org/10.3389/fmolb.2019.00079
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