ArticleNucleic acids research2023
Actin nucleators safeguard replication forks by limiting nascent strand degradation.
Article in Nucleic acids research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- The Role of Arp2/3 in End-Resection During DNA Double-Strand Break Repair.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Dispensable players: N-WASP and WASP are not crucial for homology-directed DNA repair.EMBO reports · 2026Article
- Nuclear actin and DNA replication stress regulate telomere maintenance by telomerase.Nature communications · 2025Article
- Recent advances in nuclear actin research.Nucleus (Austin, Tex.) · 2025Review
- Nucleoplasmic Lamin A/C controls replication fork restart upon stress by modulating local H3K9me3 and ADP-ribosylation levels.Nature communications · 2025Article
- Nuclear and genome dynamics underlying DNA double-strand break repair.Nature reviews. Molecular cell biology · 2025Review
- An atypical Arp2/3 complex is required for Plasmodium DNA segregation and malaria transmission.Nature microbiology · 2025Article
- Plasticity in leukocyte migration during haematopoiesis and inflammation.Journal of muscle research and cell motility · 2025Review
- Inherited deficiency of DIAPH1 identifies a DNA double strand break repair pathway regulated by γ-actin.Nature communications · 2025Article
- TORC2 inhibition triggers yeast chromosome fragmentation through misregulated Base Excision Repair of clustered oxidation events.Nature communications · 2024Article
- Regulation of Precise DNA Repair by Nuclear Actin Polymerization: A Chance for Improving Gene Therapy?Cells · 2024Review
- Replication forks associated with long nuclear actin filaments in mild stress conditions display increased dynamics.microPublication biology · 2024Article
- Genome maintenance meets mechanobiology.Chromosoma · 2024Review
- Nuclear actin polymerization rapidly mediates replication fork remodeling upon stress by limiting PrimPol activity.Nature communications · 2023Article
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Authors and funding
16 authors at 5 institutions in 3 countries.
Funding
Abstract
Accurate genome replication is essential for all life and a key mechanism of disease prevention, underpinned by the ability of cells to respond to replicative stress (RS) and protect replication forks. These responses rely on the formation of Replication Protein A (RPA)-single stranded (ss) DNA complexes, yet this process remains largely uncharacterized. Here, we establish that actin nucleation-promoting factors (NPFs) associate with replication forks, promote efficient DNA replication and facilitate association of RPA with ssDNA at sites of RS. Accordingly, their loss leads to deprotection of ssDNA at perturbed forks, impaired ATR activation, global replication defects and fork collapse. Supplying an excess of RPA restores RPA foci formation and fork protection, suggesting a chaperoning role for actin nucleators (ANs) (i.e. Arp2/3, DIAPH1) and NPFs (i.e, WASp, N-WASp) in regulating RPA availability upon RS. We also discover that β-actin interacts with RPA directly in vitro, and in vivo a hyper-depolymerizing β-actin mutant displays a heightened association with RPA and the same dysfunctional replication phenotypes as loss of ANs/NPFs, which contrasts with the phenotype of a hyper-polymerizing β-actin mutant. Thus, we identify components of actin polymerization pathways that are essential for preventing ectopic nucleolytic degradation of perturbed forks by modulating RPA activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.