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Analyzing Homologous Recombination at a Genome-Wide Level.

Authors
  • Arnould, Coline1
  • Rocher, Vincent1
  • Legube, Gaëlle2
  • 1 LBCMCP, Centre de Biologie Integrative (CBI), CNRS, Université de Toulouse, UT3, Toulouse, France. , (France)
  • 2 LBCMCP, Centre de Biologie Integrative (CBI), CNRS, Université de Toulouse, UT3, Toulouse, France. [email protected] , (France)
Type
Published Article
Journal
Methods in molecular biology
Publisher
Clifton, N.J. : Humana Press
Publication Date
Jan 01, 2021
Volume
2153
Pages
427–438
Identifiers
DOI: 10.1007/978-1-0716-0644-5_29
PMID: 32840796
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Among the types of damage, DNA double-strand breaks (DSBs) (provoked by various environmental stresses, but also during normal cell metabolic activity) are the most deleterious, as illustrated by the variety of human diseases associated with DSB repair defects. DSBs are repaired by two groups of pathways: homologous recombination (HR) and nonhomologous end joining. These pathways do not trigger the same mutational signatures, and multiple factors, such as cell cycle stage, the complexity of the lesion and also the genomic location, contribute to the choice between these repair pathways. To study the usage of the HR machinery at DSBs, we propose a genome-wide method based on the chromatin immunoprecipitation of the HR core component Rad51, followed by high-throughput sequencing.

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