ArticleThe Journal of biological chemistry2019
RecQL4 tethering on the pre-replicative complex induces unscheduled origin activation and replication stress in human cells.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 19 citations in OpenAlex.
- MCM10 and SLD-2/RECQL4 jointly activate the CMG helicase during metazoan DNA replication initiation.The EMBO journal · 2026Article
- Replication origin flexibility: a tool to mitigate the hazards of excess replication.Trends in genetics : TIG · 2026Review
- Rare genetic diseases associated with G-quadruplex-induced replication stress.Communications biology · 2026Review
- Selective interactions at pre-replication complexes categorize baseline and dormant origins.Nature communications · 2025Article
- Cyclohexylalanine-Containing α-Helical Amphipathic Peptide Targets Cardiolipin, Rescuing Mitochondrial Dysfunction in Kidney Injury.Journal of medicinal chemistry · 2024Article
- Transcription-Replication Conflicts as a Source of Genome Instability.Annual review of genetics · 2023Review
- Recognition and coacervation of G-quadruplexes by a multifunctional disordered region in RECQ4 helicase.Nature communications · 2023Article
- De novo myelodysplastic syndrome in a Rothmund-Thomson Syndrome patient with novel pathogenicBlood science (Baltimore, Md.) · 2023Article
- DNA replication initiation factor RECQ4 possesses a role in antagonizing DNA replication initiation.Nature communications · 2023Article
- Rothmund-Thomson syndrome, a disorder far from solved.Frontiers in aging · 2023Review
- High abundance of CDC45 inhibits cell proliferation through elevation of HSPA6.Cell proliferation · 2022Article
- DNA-PKcs-dependent phosphorylation of RECQL4 promotes NHEJ by stabilizing the NHEJ machinery at DNA double-strand breaks.Nucleic acids research · 2022Article
- Congenital Diseases of DNA Replication: Clinical Phenotypes and Molecular Mechanisms.International journal of molecular sciences · 2021Review
- Molecular Mechanisms of the RECQ4 Pathogenic Mutations.Frontiers in molecular biosciences · 2021Review
- A predictable conserved DNA base composition signature defines human core DNA replication origins.Nature communications · 2020Article
- Interaction between RECQL4 and OGG1 promotes repair of oxidative base lesion 8-oxoG and is regulated by SIRT1 deacetylase.Nucleic acids research · 2020Article
- Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sequential activation of DNA replication origins is precisely programmed and critical to maintaining genome stability. RecQL4, a member of the conserved RecQ family of helicases, plays an essential role in the initiation of DNA replication in mammalian cells. Here, we showed that RecQL4 protein tethered on the pre-replicative complex (pre-RC) induces early activation of late replicating origins during S phase. Tethering of RecQL4 or its N terminus on pre-RCs via fusion with Orc4 protein resulted in the recruitment of essential initiation factors, such as Mcm10, And-1, Cdc45, and GINS, increasing nascent DNA synthesis in late replicating origins during early S phase. In this origin activation process, tethered RecQL4 was able to recruit Cdc45 even in the absence of cyclin-dependent kinase (CDK) activity, whereas CDK phosphorylation of RecQL4 N terminus was required for interaction with and origin recruitment of And-1 and GINS. In addition, forced activation of replication origins by RecQL4 tethering resulted in increased replication stress and the accumulation of ssDNAs, which can be recovered by transcription inhibition. Collectively, these results suggest that recruitment of RecQL4 to replication origins is an important step for temporal activation of replication origins during S phase. Further, perturbation of replication timing control by unscheduled origin activation significantly induces replication stress, which is mostly caused by transcription-replication conflicts.
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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 OpenQuestion graph.