Cargando…

RecG controls DNA amplification at double‐strand breaks and arrested replication forks

DNA amplification is a powerful mutational mechanism that is a hallmark of cancer and drug resistance. It is therefore important to understand the fundamental pathways that cells employ to avoid over‐replicating sections of their genomes. Recent studies demonstrate that, in the absence of RecG, DNA...

Descripción completa

Detalles Bibliográficos
Autores principales: Azeroglu, Benura, Leach, David R. F.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5412681/
https://www.ncbi.nlm.nih.gov/pubmed/28155219
http://dx.doi.org/10.1002/1873-3468.12583
_version_ 1783233056197312512
author Azeroglu, Benura
Leach, David R. F.
author_facet Azeroglu, Benura
Leach, David R. F.
author_sort Azeroglu, Benura
collection PubMed
description DNA amplification is a powerful mutational mechanism that is a hallmark of cancer and drug resistance. It is therefore important to understand the fundamental pathways that cells employ to avoid over‐replicating sections of their genomes. Recent studies demonstrate that, in the absence of RecG, DNA amplification is observed at sites of DNA double‐strand break repair (DSBR) and of DNA replication arrest that are processed to generate double‐strand ends. RecG also plays a role in stabilising joint molecules formed during DSBR. We propose that RecG prevents a previously unrecognised mechanism of DNA amplification that we call reverse‐restart, which generates DNA double‐strand ends from incorrect loading of the replicative helicase at D‐loops formed by recombination, and at arrested replication forks.
format Online
Article
Text
id pubmed-5412681
institution National Center for Biotechnology Information
language English
publishDate 2017
publisher John Wiley and Sons Inc.
record_format MEDLINE/PubMed
spelling pubmed-54126812017-05-19 RecG controls DNA amplification at double‐strand breaks and arrested replication forks Azeroglu, Benura Leach, David R. F. FEBS Lett Review Articles DNA amplification is a powerful mutational mechanism that is a hallmark of cancer and drug resistance. It is therefore important to understand the fundamental pathways that cells employ to avoid over‐replicating sections of their genomes. Recent studies demonstrate that, in the absence of RecG, DNA amplification is observed at sites of DNA double‐strand break repair (DSBR) and of DNA replication arrest that are processed to generate double‐strand ends. RecG also plays a role in stabilising joint molecules formed during DSBR. We propose that RecG prevents a previously unrecognised mechanism of DNA amplification that we call reverse‐restart, which generates DNA double‐strand ends from incorrect loading of the replicative helicase at D‐loops formed by recombination, and at arrested replication forks. John Wiley and Sons Inc. 2017-02-28 2017-04 /pmc/articles/PMC5412681/ /pubmed/28155219 http://dx.doi.org/10.1002/1873-3468.12583 Text en © 2017 The Authors. FEBS Letters published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Articles
Azeroglu, Benura
Leach, David R. F.
RecG controls DNA amplification at double‐strand breaks and arrested replication forks
title RecG controls DNA amplification at double‐strand breaks and arrested replication forks
title_full RecG controls DNA amplification at double‐strand breaks and arrested replication forks
title_fullStr RecG controls DNA amplification at double‐strand breaks and arrested replication forks
title_full_unstemmed RecG controls DNA amplification at double‐strand breaks and arrested replication forks
title_short RecG controls DNA amplification at double‐strand breaks and arrested replication forks
title_sort recg controls dna amplification at double‐strand breaks and arrested replication forks
topic Review Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5412681/
https://www.ncbi.nlm.nih.gov/pubmed/28155219
http://dx.doi.org/10.1002/1873-3468.12583
work_keys_str_mv AT azeroglubenura recgcontrolsdnaamplificationatdoublestrandbreaksandarrestedreplicationforks
AT leachdavidrf recgcontrolsdnaamplificationatdoublestrandbreaksandarrestedreplicationforks