Cargando…

Analysis of repair mechanism choice during homologous recombination

Double-strand breaks (DSBs) occur frequently during cell growth. Due to the presence of repeated sequences in the genome, repair of a single DSB can result in gene conversion, translocation, deletion or tandem duplication depending on the mechanism and the sequence chosen as partner for the recombin...

Descripción completa

Detalles Bibliográficos
Autores principales: Agmon, Neta, Pur, Shiri, Liefshitz, Batia, Kupiec, Martin
Formato: Texto
Lenguaje:English
Publicado: Oxford University Press 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2731894/
https://www.ncbi.nlm.nih.gov/pubmed/19553188
http://dx.doi.org/10.1093/nar/gkp495
_version_ 1782170986935746560
author Agmon, Neta
Pur, Shiri
Liefshitz, Batia
Kupiec, Martin
author_facet Agmon, Neta
Pur, Shiri
Liefshitz, Batia
Kupiec, Martin
author_sort Agmon, Neta
collection PubMed
description Double-strand breaks (DSBs) occur frequently during cell growth. Due to the presence of repeated sequences in the genome, repair of a single DSB can result in gene conversion, translocation, deletion or tandem duplication depending on the mechanism and the sequence chosen as partner for the recombinational repair. Here, we study how yeast cells repair a single, inducible DSB when there are several potential donors to choose from, in the same chromosome and elsewhere in the genome. We systematically investigate the parameters that affect the choice of mechanism, as well as its genetic regulation. Our results indicate that intrachromosomal homologous sequences are always preferred as donors for repair. We demonstrate the occurrence of a novel tri-partite repair product that combines ectopic gene conversion and deletion. In addition, we show that increasing the distance between two repeated sequences enhances the dependence on Rad51 for colony formation after DSB repair. This is due to a role of Rad51 in the recovery from the checkpoint signal induced by the DSB. We suggest a model for the competition between the different homologous recombination pathways. Our model explains how different repair mechanisms are able to compensate for each other during DSB repair.
format Text
id pubmed-2731894
institution National Center for Biotechnology Information
language English
publishDate 2009
publisher Oxford University Press
record_format MEDLINE/PubMed
spelling pubmed-27318942009-09-10 Analysis of repair mechanism choice during homologous recombination Agmon, Neta Pur, Shiri Liefshitz, Batia Kupiec, Martin Nucleic Acids Res Genome Integrity, Repair and Replication Double-strand breaks (DSBs) occur frequently during cell growth. Due to the presence of repeated sequences in the genome, repair of a single DSB can result in gene conversion, translocation, deletion or tandem duplication depending on the mechanism and the sequence chosen as partner for the recombinational repair. Here, we study how yeast cells repair a single, inducible DSB when there are several potential donors to choose from, in the same chromosome and elsewhere in the genome. We systematically investigate the parameters that affect the choice of mechanism, as well as its genetic regulation. Our results indicate that intrachromosomal homologous sequences are always preferred as donors for repair. We demonstrate the occurrence of a novel tri-partite repair product that combines ectopic gene conversion and deletion. In addition, we show that increasing the distance between two repeated sequences enhances the dependence on Rad51 for colony formation after DSB repair. This is due to a role of Rad51 in the recovery from the checkpoint signal induced by the DSB. We suggest a model for the competition between the different homologous recombination pathways. Our model explains how different repair mechanisms are able to compensate for each other during DSB repair. Oxford University Press 2009-08 2009-06-23 /pmc/articles/PMC2731894/ /pubmed/19553188 http://dx.doi.org/10.1093/nar/gkp495 Text en © 2009 The Author(s) http://creativecommons.org/licenses/by-nc/2.0/uk/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Genome Integrity, Repair and Replication
Agmon, Neta
Pur, Shiri
Liefshitz, Batia
Kupiec, Martin
Analysis of repair mechanism choice during homologous recombination
title Analysis of repair mechanism choice during homologous recombination
title_full Analysis of repair mechanism choice during homologous recombination
title_fullStr Analysis of repair mechanism choice during homologous recombination
title_full_unstemmed Analysis of repair mechanism choice during homologous recombination
title_short Analysis of repair mechanism choice during homologous recombination
title_sort analysis of repair mechanism choice during homologous recombination
topic Genome Integrity, Repair and Replication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2731894/
https://www.ncbi.nlm.nih.gov/pubmed/19553188
http://dx.doi.org/10.1093/nar/gkp495
work_keys_str_mv AT agmonneta analysisofrepairmechanismchoiceduringhomologousrecombination
AT purshiri analysisofrepairmechanismchoiceduringhomologousrecombination
AT liefshitzbatia analysisofrepairmechanismchoiceduringhomologousrecombination
AT kupiecmartin analysisofrepairmechanismchoiceduringhomologousrecombination