Abstract
DNA double-strand breaks (DSB) can arise during DNA replication, or after exposure to DNA-damaging agents, and their correct repair is fundamental for cell survival and genomic stability. Here, we show that the Smc5-Smc6 complex is recruited to DSBs de novo to support their repair by homologous recombination between sister chromatids. In addition, we demonstrate that Smc5-Smc6 is necessary to suppress gross chromosomal rearrangements. Our findings show that the Smc5-Smc6 complex is essential for genome stability as it promotes repair of DSBs by error-free sister-chromatid recombination (SCR), thereby suppressing inappropriate non-sister recombination events.
MeSH Terms
Cell Cycle Proteins/physiology
DNA/metabolism
DNA Damage
Deoxyribonucleases, Type II Site-Specific/metabolism
Genomic Instability
Saccharomyces cerevisiae/genetics,physiology
Saccharomyces cerevisiae Proteins/physiology
Sister Chromatid Exchange
Chemicals
Cell Cycle Proteins
SMC5 protein, S cerevisiae
SMC6 protein, S cerevisiae
Saccharomyces cerevisiae Proteins
DNA
SCEI protein, S cerevisiae
Deoxyribonucleases, Type II Site-Specific
Authors & Affiliations
24 authors, click to expand affiliations / ORCID
De Piccoli Giacomo
Cell Cycle Group, MRC Clinical Sciences Centre, Imperial College London, Du Cane Road, London W12 0NN, UK.
Cortes-Ledesma Felipe
Ira Gregory
Torres-Rosell Jordi
Uhle Stefan
Farmer Sarah
Hwang Ji-Young
Machin Felix
Ceschia Audrey
McAleenan Alexandra
Cordon-Preciado Violeta
Clemente-Blanco Andrés
Vilella-Mitjana Felip
Ullal Pranav
Jarmuz Adam
Leitao Beatriz
Bressan Debra
Dotiwala Farokh
Papusha Alma
Zhao Xiaolan
Myung Kyungjae
Haber James E
Aguilera Andrés
Aragón Luis
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