Rad51 recombinase prevents Mre11 nuclease-dependent degradation and excessive PrimPol-mediated elongation of nascent DNA after UV irradiation
Copyright policy )Rad51 recombinase prevents Mre11 nuclease-dependent degradation and excessive PrimPol-mediated elongation of nascent DNA after UV irradiation
Significance Pathways that promote DNA replication across replication barriers are central for cell survival. Herein, we report that in UV-irradiated cells lacking the Rad51 recombinase (Rad51), the DNA replication choreography is profoundly altered. We detected excessive degradation of nascent DNA followed by dysregulated elongation of DNA across UV barriers. PrimPol, a DNA polymerase with primase activity, promoted excessive elongation of nascent DNA, thus suggesting the accumulation of discontinuous replication tracks in Rad51-depleted cells. The altered DNA replication choreography in Rad51-knockdown samples resulted in the accumulation of replication stress markers and cell death. Hence, Rad51 promotes multiple, biologically relevant events at ongoing forks that encounter UV-damaged replication templates.
DNA Replication, MRE11 Homologue Protein, Cell Death, DNA Repair, Cell Survival, Ultraviolet Rays, Cell Cycle, Dose-Response Relationship, Radiation, DNA, DNA Primase, DNA-Directed DNA Polymerase, Multifunctional Enzymes, DNA-Binding Proteins, Cell Line, Tumor, Disease Progression, Humans, DNA Breaks, Double-Stranded, Rad51 Recombinase, RNA, Small Interfering, HeLa Cells
DNA Replication, MRE11 Homologue Protein, Cell Death, DNA Repair, Cell Survival, Ultraviolet Rays, Cell Cycle, Dose-Response Relationship, Radiation, DNA, DNA Primase, DNA-Directed DNA Polymerase, Multifunctional Enzymes, DNA-Binding Proteins, Cell Line, Tumor, Disease Progression, Humans, DNA Breaks, Double-Stranded, Rad51 Recombinase, RNA, Small Interfering, HeLa Cells
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