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Stress Activated Protein Kinase Pathway Modulates Homologous Recombination in Fission Yeast

Rad52 is a key player in homologous recombination (HR), a DNA repair pathway that is dedicated to double strand breaks repair and recovery of perturbed replication forks. Here we show that fission yeast Rad52 homologue is phosphorylated when S phase cells are exposed to ROS inducers such as ultravio...

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Autores principales: Bellini, Angela, Girard, Pierre-Marie, Lambert, Sarah, Tessier, Ludovic, Sage, Evelyne, Francesconi, Stefania
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3485339/
https://www.ncbi.nlm.nih.gov/pubmed/23118915
http://dx.doi.org/10.1371/journal.pone.0047987
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author Bellini, Angela
Girard, Pierre-Marie
Lambert, Sarah
Tessier, Ludovic
Sage, Evelyne
Francesconi, Stefania
author_facet Bellini, Angela
Girard, Pierre-Marie
Lambert, Sarah
Tessier, Ludovic
Sage, Evelyne
Francesconi, Stefania
author_sort Bellini, Angela
collection PubMed
description Rad52 is a key player in homologous recombination (HR), a DNA repair pathway that is dedicated to double strand breaks repair and recovery of perturbed replication forks. Here we show that fission yeast Rad52 homologue is phosphorylated when S phase cells are exposed to ROS inducers such as ultraviolet A radiation or hydrogen peroxide, but not to ultraviolet C or camptothecin. Phosphorylation does not depend on kinases Chk1, Rad3, Tel1 or Cdc2, but depends on a functional stress activated protein kinase (SAPK) pathway and can be partially prevented by anti-oxidant treatment. Indeed, cells lacking Sty1, the major fission yeast MAP kinase of the SAPK pathway, do not display Rad52 phosphorylation and have UVA induced Rad52 foci that persist longer if compared to wild type cells. In addition, spontaneous intrachromosomal HR is diminished in cells lacking Sty1 and, more precisely, gene conversion is affected. Moreover, HR induced by site-specific arrest of replication forks is twice less efficient in cells that do not express Sty1. Importantly, impairing HR by deletion of the gene encoding the recombinase Rhp51 leads to Sty1 dependent Rad52 phosphorylation. Thus, SAPK pathway impinges on early step of HR through phosphorylation of Rad52 in cells challenged by oxidative stress or lacking Rhp51 and is required to promote spontaneous gene conversion and recovery from blocked replication forks.
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spelling pubmed-34853392012-11-01 Stress Activated Protein Kinase Pathway Modulates Homologous Recombination in Fission Yeast Bellini, Angela Girard, Pierre-Marie Lambert, Sarah Tessier, Ludovic Sage, Evelyne Francesconi, Stefania PLoS One Research Article Rad52 is a key player in homologous recombination (HR), a DNA repair pathway that is dedicated to double strand breaks repair and recovery of perturbed replication forks. Here we show that fission yeast Rad52 homologue is phosphorylated when S phase cells are exposed to ROS inducers such as ultraviolet A radiation or hydrogen peroxide, but not to ultraviolet C or camptothecin. Phosphorylation does not depend on kinases Chk1, Rad3, Tel1 or Cdc2, but depends on a functional stress activated protein kinase (SAPK) pathway and can be partially prevented by anti-oxidant treatment. Indeed, cells lacking Sty1, the major fission yeast MAP kinase of the SAPK pathway, do not display Rad52 phosphorylation and have UVA induced Rad52 foci that persist longer if compared to wild type cells. In addition, spontaneous intrachromosomal HR is diminished in cells lacking Sty1 and, more precisely, gene conversion is affected. Moreover, HR induced by site-specific arrest of replication forks is twice less efficient in cells that do not express Sty1. Importantly, impairing HR by deletion of the gene encoding the recombinase Rhp51 leads to Sty1 dependent Rad52 phosphorylation. Thus, SAPK pathway impinges on early step of HR through phosphorylation of Rad52 in cells challenged by oxidative stress or lacking Rhp51 and is required to promote spontaneous gene conversion and recovery from blocked replication forks. Public Library of Science 2012-10-31 /pmc/articles/PMC3485339/ /pubmed/23118915 http://dx.doi.org/10.1371/journal.pone.0047987 Text en © 2012 Bellini et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Bellini, Angela
Girard, Pierre-Marie
Lambert, Sarah
Tessier, Ludovic
Sage, Evelyne
Francesconi, Stefania
Stress Activated Protein Kinase Pathway Modulates Homologous Recombination in Fission Yeast
title Stress Activated Protein Kinase Pathway Modulates Homologous Recombination in Fission Yeast
title_full Stress Activated Protein Kinase Pathway Modulates Homologous Recombination in Fission Yeast
title_fullStr Stress Activated Protein Kinase Pathway Modulates Homologous Recombination in Fission Yeast
title_full_unstemmed Stress Activated Protein Kinase Pathway Modulates Homologous Recombination in Fission Yeast
title_short Stress Activated Protein Kinase Pathway Modulates Homologous Recombination in Fission Yeast
title_sort stress activated protein kinase pathway modulates homologous recombination in fission yeast
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3485339/
https://www.ncbi.nlm.nih.gov/pubmed/23118915
http://dx.doi.org/10.1371/journal.pone.0047987
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