ArticleNucleic acids research2024
Replication fork stalling in late S-phase elicits nascent strand degradation by DNA mismatch repair.
Article in Nucleic acids research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Replication associated nuclear DNA mismatch repair across kingdoms.Biochemical Society transactions · 2026Review
- Chicken lncRNA-9802 Induces the S Phase Arrest in the T Lymphocyte Cells Infected by Marek's Disease Virus via the TP53BP1/p53/p21 Pathway.Veterinary sciences · 2026Article
- Therapy-associated mutagenesis at CTCF binding sites is shaped by chromatin context and DNA repair capacity.bioRxiv : the preprint server for biology · 2026Article
- DNA replication timing reveals genome-wide features of transcription and fragility.Nature communications · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Eukaryotic chromosomal replication occurs in a segmented, temporal manner wherein open euchromatin and compact heterochromatin replicate during early and late S-phase respectively. Using single molecule DNA fiber analyses coupled with cell synchronization, we find that newly synthesized strands remain stable at perturbed forks in early S-phase. Unexpectedly, stalled forks are susceptible to nucleolytic digestion during late replication resulting in defective fork restart. This inherent vulnerability to nascent strand degradation is dependent on fork reversal enzymes and resection nucleases MRE11, DNA2 and EXO1. Inducing chromatin compaction elicits digestion of nascent DNA in response to fork stalling due to reduced association of RAD51 with nascent DNA. Furthermore, RAD51 occupancy at stalled forks in late S-phase is diminished indicating that densely packed chromatin limits RAD51 accessibility to mediate replication fork protection. Genetic analyses reveal that susceptibility of late replicating forks to nascent DNA digestion is dependent on EXO1 via DNA mismatch repair (MMR) and that the BRCA2-mediated replication fork protection blocks MMR from degrading nascent DNA. Overall, our findings illustrate differential regulation of fork protection between early and late replication and demonstrate nascent strand degradation as a critical determinant of heterochromatin instability in response to replication stress.
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Registered trials
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