ArticleeLife2015
Cdc6 ATPase activity disengages Cdc6 from the pre-replicative complex to promote DNA replication.
Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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
24 citing papers in PubMed, 33 citations in OpenAlex.
- A lethal ORC ATPase mutation is suppressed by alterations in ORC and RNA Pol II transcription components.PloS one · 2026Article
- The DNA replication machinery transmits dual signals to prevent unscheduled licensing and execution of centrosome duplication.Nature communications · 2025Article
- Reconstitution of human DNA licensing and the structural and functional analysis of key intermediates.Nature communications · 2025Article
- MCM2-7 ring closure involves the Mcm5 C-terminus and triggers Mcm4 ATP hydrolysis.Nature communications · 2025Article
- Gene Expression Analysis of Yeast Strains with a Nonsense Mutation in the eRF3-Coding Gene Highlights Possible Mechanisms of Adaptation.International journal of molecular sciences · 2024Article
- The expanding genetic and clinical landscape associated with Meier-Gorlin syndrome.European journal of human genetics : EJHG · 2023Review
- Changing protein-DNA interactions promote ORC binding-site exchange during replication origin licensing.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Changing protein-DNA interactions promote ORC binding site exchange during replication origin licensing.bioRxiv : the preprint server for biology · 2023Article
- Mechanisms of hexameric helicases.Critical reviews in biochemistry and molecular biology · 2021Review
- The structure of ORC-Cdc6 on an origin DNA reveals the mechanism of ORC activation by the replication initiator Cdc6.Nature communications · 2021Article
- Article
- Molecular mechanisms of eukaryotic origin initiation, replication fork progression, and chromatin maintenance.The Biochemical journal · 2020Article
- A structural view of the initiators for chromosome replication.Current opinion in structural biology · 2018Review
- Yeast heterochromatin regulators Sir2 and Sir3 act directly at euchromatic DNA replication origins.PLoS genetics · 2018Article
- Expression and prognostic significance of MCM-3 and MCM-7 in salivary adenoid cystic carcinoma.International journal of clinical and experimental pathology · 2018Article
- Article
- MCM interference during licensing of DNA replication in Xenopus egg extracts-Possible Role of a C-terminal region of MCM3.Cell cycle (Georgetown, Tex.) · 2018Article
- The High-Affinity Interaction between ORC and DNA that Is Required for Replication Licensing Is Inhibited by 2-Arylquinolin-4-Amines.Cell chemical biology · 2017Article
- Mechanisms and regulation of DNA replication initiation in eukaryotes.Critical reviews in biochemistry and molecular biology · 2017Review
- Structural basis of Mcm2-7 replicative helicase loading by ORC-Cdc6 and Cdt1.Nature structural & molecular biology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
To initiate DNA replication, cells first load an MCM helicase double hexamer at origins in a reaction requiring ORC, Cdc6, and Cdt1, also called pre-replicative complex (pre-RC) assembly. The essential mechanistic role of Cdc6 ATP hydrolysis in this reaction is still incompletely understood. Here, we show that although Cdc6 ATP hydrolysis is essential to initiate DNA replication, it is not essential for MCM loading. Using purified proteins, an ATPase-defective Cdc6 mutant 'Cdc6-E224Q' promoted MCM loading on DNA. Cdc6-E224Q also promoted MCM binding at origins in vivo but cells remained blocked in G1-phase. If after loading MCM, Cdc6-E224Q was degraded, cells entered an apparently normal S-phase and replicated DNA, a phenotype seen with two additional Cdc6 ATPase-defective mutants. Cdc6 ATP hydrolysis is therefore required for Cdc6 disengagement from the pre-RC after helicase loading to advance subsequent steps in helicase activation in vivo.
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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.