ArticleNature communications2025
Selective interactions at pre-replication complexes categorize baseline and dormant origins.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Tumor-targeted top1 inhibitor delivery with optimized parp inhibition in advanced solid tumors: a phase i trial of gapped scheduling.Nature communications · 2025Trial
- MCM10 and SLD-2/RECQL4 jointly activate the CMG helicase during metazoan DNA replication initiation.The EMBO journal · 2026Article
- MCM3 Safeguards Neural Progenitor Maintenance and Cortical Development Against Replication-Associated Stress.Molecular neurobiology · 2026Article
- Replication origin flexibility: a tool to mitigate the hazards of excess replication.Trends in genetics : TIG · 2026Review
- Dynamic regulation of origin firing factors links CDK activity to dormant origin activation.Nature communications · 2026Article
- ATR and TopBP1 oppose to control dormant origin activity and global replication dynamics, providing a first defense against replication stress.Nucleic acids research · 2026Article
- Minute amounts of helicase-deficient truncated RECQL4 are sufficient for DNA replication.EMBO reports · 2026Article
- Impact of Tau overexpression on DNA replication dynamics in centromeres of human neural progenitor cells.iScience · 2026Article
- Regulated TRESLIN-MTBP loading governs initiation zones and replication timing in human DNA replication.Nature communications · 2025Article
- Cell cycle-dependent TICRR/TRESLIN and MTBP chromatin binding mechanisms and patterns.Genome biology · 2025Article
- Due-B Is dispensable for early development and genome duplication in vertebrates.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
DNA synthesis in metazoans initiates within a select group of replication origins (baseline origins), whereas other (dormant) origins do not initiate replication despite recruiting apparently indistinguishable pre-replication complexes. Dormant origins are activated as backups when DNA synthesis stalls, allowing for complete genome duplication, yet it is unclear how cells selectively differentiate between baseline and dormant origins. We report here that during unperturbed cell proliferation, dormant origins selectively bind phosphorylated RecQL4 (pRecQL4), a member of the RecQ helicase family mutated in Rothmund-Thomson, RAPADILINO and Baller-Gerold syndromes. Origin-bound pRecQL4 prevents the binding of an essential replication initiation complex, MTBP-TICRR/TRESLIN, to dormant origins, thus restricting replication initiation to baseline origins. When cells encounter replication stress, pRecQL4 is required for the dissociation of the MTBP-TICRR/TRESLIN complex from chromatin, which, in turn, facilitates the subsequent redistribution of MTBP-TICRR/TRESLIN to both baseline and dormant origins and allows recovery from replication inhibition. Thus, the interactions between the MTBP-TICRR/TRESLIN complex and pRecQL4 at replication origins are critical for replication origin choice and facilitate recovery from replication stress.
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