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RECQ5 Helicase Cooperates with MUS81 Endonuclease in Processing Stalled Replication Forks at Common Fragile Sites during Mitosis.

Molecular cell | Jun 1, 2017

The MUS81-EME1 endonuclease cleaves late replication intermediates at common fragile sites (CFSs) during early mitosis to trigger DNA-repair synthesis that ensures faithful chromosome segregation. Here, we show that these DNA transactions are promoted by RECQ5 DNA helicase in a manner dependent on its Ser727 phosphorylation by CDK1. Upon replication stress, RECQ5 associates with CFSs in early mitosis through its physical interaction with MUS81 and promotes MUS81-dependent mitotic DNA synthesis. RECQ5 depletion or mutational inactivation of its ATP-binding site, RAD51-interacting domain, or phosphorylation site causes excessive binding of RAD51 to CFS loci and impairs CFS expression. This leads to defective chromosome segregation and accumulation of CFS-associated DNA damage in G1 cells. Biochemically, RECQ5 alleviates the inhibitory effect of RAD51 on 3'-flap DNA cleavage by MUS81-EME1 through its RAD51 filament disruption activity. These data suggest that RECQ5 removes RAD51 filaments stabilizing stalled replication forks at CFSs and hence facilitates CFS cleavage by MUS81-EME1.

Pubmed ID: 28575661 RIS Download

Mesh terms: Binding Sites | Chromosomal Instability | Chromosome Fragile Sites | Chromosome Segregation | Cyclin-Dependent Kinases | DNA | DNA Damage | DNA Repair | DNA-Binding Proteins | Endodeoxyribonucleases | Endonucleases | HEK293 Cells | HeLa Cells | Humans | Mitosis | Phosphorylation | Protein Binding | RNA Interference | Rad51 Recombinase | RecQ Helicases | Replication Origin | Time Factors | Transfection

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