ArticleThe Journal of cell biology2012
The dynamics of replication licensing in live Caenorhabditis elegans embryos.
Article in The Journal of cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
55 citing papers in PubMed, 73 citations in OpenAlex.
- MCM10 and SLD-2/RECQL4 jointly activate the CMG helicase during metazoan DNA replication initiation.The EMBO journal · 2026Article
- Functional dissection of the conserved C. elegans LEM-3/ANKLE1 nuclease reveals a crucial requirement for the LEM-like and GIY-YIG domains for DNA bridge processing.Nucleic acids research · 2025Article
- The replicative helicase CMG is required for the divergence of cell fates during asymmetric cell division in vivo.Nature communications · 2024Article
- MCM2-7 loading-dependent ORC release ensures genome-wide origin licensing.Nature communications · 2024Article
- Distinct roles of Arabidopsis ORC1 proteins in DNA replication and heterochromatic H3K27me1 deposition.Nature communications · 2023Article
- Isolation, profiling, and tracking of extracellular vesicle cargo in Caenorhabditis elegans.Current biology : CB · 2022Article
- The proteome of developing barley anthers during meiotic prophase I.Journal of experimental botany · 2022Article
- Review
- Molecular determinants of phase separation foreLife · 2021Article
- RbAp46/48LIN-53 and HAT-1 are required for initial CENP-AHCP-3 deposition and de novo holocentromere formation on artificial chromosomes in Caenorhabditis elegans embryos.Nucleic acids research · 2021Article
- The capacity of origins to load MCM establishes replication timing patterns.PLoS genetics · 2021Article
- Loss of histone H3.3 results in DNA replication defects and altered origin dynamics inGenome research · 2020Article
- Meiotic Double-Strand Break Processing and Crossover Patterning Are Regulated in a Sex-Specific Manner by BRCA1-BARD1 inGenetics · 2020Article
- A new class of disordered elements controls DNA replication through initiator self-assembly.eLife · 2019Article
- TRAIP drives replisome disassembly and mitotic DNA repair synthesis at sites of incomplete DNA replication.eLife · 2019Article
- Tissue-Specific Split sfGFP System for Streamlined Expression of GFP Tagged Proteins in theG3 (Bethesda, Md.) · 2019Article
- Spatial and temporal resolution of mORC4 fluorescent variants reveals structural requirements for achieving higher order self-association and pronuclei entry.Methods and applications in fluorescence · 2019Article
- Developmental Control of the Cell Cycle: Insights fromGenetics · 2019Review
- Multiple Mechanisms Inactivate the LIN-41 RNA-Binding Protein To Ensure a Robust Oocyte-to-Embryo Transition inGenetics · 2018Article
- The tumor suppressor BRCA1-BARD1 complex localizes to the synaptonemal complex and regulates recombination under meiotic dysfunction in Caenorhabditis elegans.PLoS genetics · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Accurate DNA replication requires proper regulation of replication licensing, which entails loading MCM-2-7 onto replication origins. In this paper, we provide the first comprehensive view of replication licensing in vivo, using video microscopy of Caenorhabditis elegans embryos. As expected, MCM-2-7 loading in late M phase depended on the prereplicative complex (pre-RC) proteins: origin recognition complex (ORC), CDC-6, and CDT-1. However, many features we observed have not been described before: GFP-ORC-1 bound chromatin independently of ORC-2-5, and CDC-6 bound chromatin independently of ORC, whereas CDT-1 and MCM-2-7 DNA binding was interdependent. MCM-3 chromatin loading was irreversible, but CDC-6 and ORC turned over rapidly, consistent with ORC/CDC-6 loading multiple MCM-2-7 complexes. MCM-2-7 chromatin loading further reduced ORC and CDC-6 DNA binding. This dynamic behavior creates a feedback loop allowing ORC/CDC-6 to repeatedly load MCM-2-7 and distribute licensed origins along chromosomal DNA. During S phase, ORC and CDC-6 were excluded from nuclei, and DNA was overreplicated in export-defective cells. Thus, nucleocytoplasmic compartmentalization of licensing factors ensures that DNA replication occurs only once.
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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.