ArticleNucleic acids research2013
Activation of a human chromosomal replication origin by protein tethering.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Due-B Is dispensable for early development and genome duplication in vertebrates.bioRxiv : the preprint server for biology · 2025Article
- Multifunctional acyltransferase HBO1: a key regulatory factor for cellular functions.Cellular & molecular biology letters · 2024Review
- Microsatellite break-induced replication generates highly mutagenized extrachromosomal circular DNAs.NAR cancer · 2024Article
- Article
- Stable G-quadruplex DNA structures promote replication-dependent genome instability.The Journal of biological chemistry · 2022Article
- Replication stress at microsatellites causes DNA double-strand breaks and break-induced replication.The Journal of biological chemistry · 2020Article
- Deciphering structure, function and mechanism of lysine acetyltransferase HBO1 in protein acetylation, transcription regulation, DNA replication and its oncogenic properties in cancer.Cellular and molecular life sciences : CMLS · 2020Review
- Deficiency of the Fanconi anemia E2 ubiqitin conjugase UBE2T only partially abrogates Alu-mediated recombination in a new model of homology dependent recombination.Nucleic acids research · 2019Article
- Phosphorylated SIRT1 associates with replication origins to prevent excess replication initiation and preserve genomic stability.Nucleic acids research · 2017Article
- Order from clutter: selective interactions at mammalian replication origins.Nature reviews. Genetics · 2017Review
- Regulation of Replication Origins.Advances in experimental medicine and biology · 2017Review
- FANCJ is essential to maintain microsatellite structure genome-wide during replication stress.Nucleic acids research · 2016Article
- Replication origins: determinants or consequences of nuclear organization?Current opinion in genetics & development · 2016Review
- Reduced cohesin destabilizes high-level gene amplification by disrupting pre-replication complex bindings in human cancers with chromosomal instability.Nucleic acids research · 2016Article
- BRPF3-HBO1 regulates replication origin activation and histone H3K14 acetylation.The EMBO journal · 2016Article
- A Role of hIPI3 in DNA Replication Licensing in Human Cells.PloS one · 2016Article
- Initiation of replication in Xenopus egg extracts at a spatially defined origin.Cell cycle (Georgetown, Tex.) · 2015Article
- Protein phosphatase 2A and Cdc7 kinase regulate the DNA unwinding element-binding protein in replication initiation.The Journal of biological chemistry · 2014Article
- Chromatin structure and replication origins: determinants of chromosome replication and nuclear organization.Journal of molecular biology · 2014Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The specification of mammalian chromosomal replication origins is incompletely understood. To analyze the assembly and activation of prereplicative complexes (pre-RCs), we tested the effects of tethered binding of chromatin acetyltransferases and replication proteins on chromosomal c-myc origin deletion mutants containing a GAL4-binding cassette. GAL4(DBD) (DNA binding domain) fusions with Orc2, Cdt1, E2F1 or HBO1 coordinated the recruitment of the Mcm7 helicase subunit, the DNA unwinding element (DUE)-binding protein DUE-B and the minichromosome maintenance (MCM) helicase activator Cdc45 to the replicator, and restored origin activity. In contrast, replication protein binding and origin activity were not stimulated by fusion protein binding in the absence of flanking c-myc DNA. Substitution of the GAL4-binding site for the c-myc replicator DUE allowed Orc2 and Mcm7 binding, but eliminated origin activity, indicating that the DUE is essential for pre-RC activation. Additionally, tethering of DUE-B was not sufficient to recruit Cdc45 or activate pre-RCs formed in the absence of a DUE. These results show directly in a chromosomal background that chromatin acetylation, Orc2 or Cdt1 suffice to recruit all downstream replication initiation activities to a prospective origin, and that chromosomal origin activity requires singular DNA sequences.
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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 OpenQuestion graph.