Break-induced replication promotes formation of lethal joint molecules dissolved by Srs2

Break-induced replication (BIR) is a double-strand break repair pathway that can lead to genomic instability. Here the authors show that the absence of Srs2 helicase during BIR leads to uncontrolled binding of Rad51 to single-stranded DNA, which promotes the formation of toxic intermediates that nee...

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Main Authors: Rajula Elango, Ziwei Sheng, Jessica Jackson, Jenna DeCata, Younis Ibrahim, Nhung T. Pham, Diana H. Liang, Cynthia J. Sakofsky, Alessandro Vindigni, Kirill S. Lobachev, Grzegorz Ira, Anna Malkova
Format: Article
Language:English
Published: Nature Portfolio 2017-11-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-017-01987-2
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author Rajula Elango
Ziwei Sheng
Jessica Jackson
Jenna DeCata
Younis Ibrahim
Nhung T. Pham
Diana H. Liang
Cynthia J. Sakofsky
Alessandro Vindigni
Kirill S. Lobachev
Grzegorz Ira
Anna Malkova
author_facet Rajula Elango
Ziwei Sheng
Jessica Jackson
Jenna DeCata
Younis Ibrahim
Nhung T. Pham
Diana H. Liang
Cynthia J. Sakofsky
Alessandro Vindigni
Kirill S. Lobachev
Grzegorz Ira
Anna Malkova
author_sort Rajula Elango
collection DOAJ
description Break-induced replication (BIR) is a double-strand break repair pathway that can lead to genomic instability. Here the authors show that the absence of Srs2 helicase during BIR leads to uncontrolled binding of Rad51 to single-stranded DNA, which promotes the formation of toxic intermediates that need to be resolved by Mus81 or Yen1.
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spelling doaj.art-9b329335ec744672ad3e5e67091d04d52022-12-21T22:54:42ZengNature PortfolioNature Communications2041-17232017-11-018111310.1038/s41467-017-01987-2Break-induced replication promotes formation of lethal joint molecules dissolved by Srs2Rajula Elango0Ziwei Sheng1Jessica Jackson2Jenna DeCata3Younis Ibrahim4Nhung T. Pham5Diana H. Liang6Cynthia J. Sakofsky7Alessandro Vindigni8Kirill S. Lobachev9Grzegorz Ira10Anna Malkova11Department of Biology, University of IowaSchool of Biological Sciences and Institute for Bioengineering and Bioscience, Georgia Institute of TechnologyEdward A Doisy Department of Biochemistry and Molecular Biology, Saint Louis University School of MedicineDepartment of Biology, University of IowaDepartment of Biology, University of IowaDepartment of Molecular & Human Genetics, Baylor College of MedicineDepartment of Molecular & Human Genetics, Baylor College of MedicineDepartment of Biology, University of IowaEdward A Doisy Department of Biochemistry and Molecular Biology, Saint Louis University School of MedicineSchool of Biological Sciences and Institute for Bioengineering and Bioscience, Georgia Institute of TechnologyDepartment of Molecular & Human Genetics, Baylor College of MedicineDepartment of Biology, University of IowaBreak-induced replication (BIR) is a double-strand break repair pathway that can lead to genomic instability. Here the authors show that the absence of Srs2 helicase during BIR leads to uncontrolled binding of Rad51 to single-stranded DNA, which promotes the formation of toxic intermediates that need to be resolved by Mus81 or Yen1.https://doi.org/10.1038/s41467-017-01987-2
spellingShingle Rajula Elango
Ziwei Sheng
Jessica Jackson
Jenna DeCata
Younis Ibrahim
Nhung T. Pham
Diana H. Liang
Cynthia J. Sakofsky
Alessandro Vindigni
Kirill S. Lobachev
Grzegorz Ira
Anna Malkova
Break-induced replication promotes formation of lethal joint molecules dissolved by Srs2
Nature Communications
title Break-induced replication promotes formation of lethal joint molecules dissolved by Srs2
title_full Break-induced replication promotes formation of lethal joint molecules dissolved by Srs2
title_fullStr Break-induced replication promotes formation of lethal joint molecules dissolved by Srs2
title_full_unstemmed Break-induced replication promotes formation of lethal joint molecules dissolved by Srs2
title_short Break-induced replication promotes formation of lethal joint molecules dissolved by Srs2
title_sort break induced replication promotes formation of lethal joint molecules dissolved by srs2
url https://doi.org/10.1038/s41467-017-01987-2
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