Processing of DNA Double-Strand Breaks by the MRX Complex in a Chromatin Context

DNA double-strand breaks (DSBs) are highly cytotoxic lesions that must be repaired to ensure genomic stability and avoid cell death. The cellular response to DSBs is initiated by the evolutionarily conserved Mre11-Rad50-Xrs2/NBS1 (MRX/MRN) complex that has structural and catalytic functions. Further...

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Autores principales: Casari, Erika, Rinaldi, Carlo, Marsella, Antonio, Gnugnoli, Marco, Colombo, Chiara Vittoria, Bonetti, Diego, Longhese, Maria Pia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Molecular Biosciences
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6567933/
https://www.ncbi.nlm.nih.gov/pubmed/31231660
http://dx.doi.org/10.3389/fmolb.2019.00043
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author Casari, Erika
Rinaldi, Carlo
Marsella, Antonio
Gnugnoli, Marco
Colombo, Chiara Vittoria
Bonetti, Diego
Longhese, Maria Pia
author_facet Casari, Erika
Rinaldi, Carlo
Marsella, Antonio
Gnugnoli, Marco
Colombo, Chiara Vittoria
Bonetti, Diego
Longhese, Maria Pia
author_sort Casari, Erika
collection PubMed
description DNA double-strand breaks (DSBs) are highly cytotoxic lesions that must be repaired to ensure genomic stability and avoid cell death. The cellular response to DSBs is initiated by the evolutionarily conserved Mre11-Rad50-Xrs2/NBS1 (MRX/MRN) complex that has structural and catalytic functions. Furthermore, it is responsible for DSB signaling through the activation of the checkpoint kinase Tel1/ATM. Here, we review functions and regulation of the MRX/MRN complex in DSB processing in a chromatin context, as well as its interplay with Tel1/ATM.
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spelling pubmed-65679332019-06-21 Processing of DNA Double-Strand Breaks by the MRX Complex in a Chromatin Context Casari, Erika Rinaldi, Carlo Marsella, Antonio Gnugnoli, Marco Colombo, Chiara Vittoria Bonetti, Diego Longhese, Maria Pia Front Mol Biosci Molecular Biosciences DNA double-strand breaks (DSBs) are highly cytotoxic lesions that must be repaired to ensure genomic stability and avoid cell death. The cellular response to DSBs is initiated by the evolutionarily conserved Mre11-Rad50-Xrs2/NBS1 (MRX/MRN) complex that has structural and catalytic functions. Furthermore, it is responsible for DSB signaling through the activation of the checkpoint kinase Tel1/ATM. Here, we review functions and regulation of the MRX/MRN complex in DSB processing in a chromatin context, as well as its interplay with Tel1/ATM. Frontiers Media S.A. 2019-06-07 /pmc/articles/PMC6567933/ /pubmed/31231660 http://dx.doi.org/10.3389/fmolb.2019.00043 Text en Copyright © 2019 Casari, Rinaldi, Marsella, Gnugnoli, Colombo, Bonetti and Longhese. 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
Casari, Erika
Rinaldi, Carlo
Marsella, Antonio
Gnugnoli, Marco
Colombo, Chiara Vittoria
Bonetti, Diego
Longhese, Maria Pia
Processing of DNA Double-Strand Breaks by the MRX Complex in a Chromatin Context
title Processing of DNA Double-Strand Breaks by the MRX Complex in a Chromatin Context
title_full Processing of DNA Double-Strand Breaks by the MRX Complex in a Chromatin Context
title_fullStr Processing of DNA Double-Strand Breaks by the MRX Complex in a Chromatin Context
title_full_unstemmed Processing of DNA Double-Strand Breaks by the MRX Complex in a Chromatin Context
title_short Processing of DNA Double-Strand Breaks by the MRX Complex in a Chromatin Context
title_sort processing of dna double-strand breaks by the mrx complex in a chromatin context
topic Molecular Biosciences
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6567933/
https://www.ncbi.nlm.nih.gov/pubmed/31231660
http://dx.doi.org/10.3389/fmolb.2019.00043
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