ArticleMolecular biology of the cell1999
Phosphorylation controls timing of Cdc6p destruction: A biochemical analysis.
Article in Molecular biology of the cell, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 153 citations in OpenAlex.
- Cell cycle regulation has shaped replication origins in budding yeast.Nature structural & molecular biology · 2025Article
- Regulation of replication origin licensing by ORC phosphorylation reveals a two-step mechanism for Mcm2-7 ring closing.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Regulation of replication origin licensing by ORC phosphorylation reveals a two-step mechanism for Mcm2-7 ring closing.bioRxiv : the preprint server for biology · 2023Article
- Control of pre-replicative complex during the division cycle in Chlamydomonas reinhardtii.PLoS genetics · 2021Article
- Review
- The Cdk2-c-Myc-miR-571 Axis Regulates DNA Replication and Genomic Stability by Targeting Geminin.Cancer research · 2019Article
- A comprehensive, mechanistically detailed, and executable model of the cell division cycle in Saccharomyces cerevisiae.Nature communications · 2019Article
- Control of Eukaryotic DNA Replication Initiation-Mechanisms to Ensure Smooth Transitions.Genes · 2019Review
- Article
- Nuclear DNA Replication in Trypanosomatids: There Are No Easy Methods for Solving Difficult Problems.Trends in parasitology · 2017Review
- A new cell cycle checkpoint that senses plasma membrane/cell wall damage in budding yeast.BioEssays : news and reviews in molecular, cellular and developmental biology · 2017Review
- Regulation and Function of Cdt1; A Key Factor in Cell Proliferation and Genome Stability.Genes · 2016Review
- Plasma membrane/cell wall perturbation activates a novel cell cycle checkpoint during G1 in Saccharomyces cerevisiae.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- SCF(Cyclin F)-dependent degradation of CDC6 suppresses DNA re-replication.Nature communications · 2016Article
- Cdc6 degradation requires phosphodegron created by GSK-3 and Cdk1 for SCFCdc4 recognition in Saccharomyces cerevisiae.Molecular biology of the cell · 2015Article
- Review
- Switch on the engine: how the eukaryotic replicative helicase MCM2-7 becomes activated.Chromosoma · 2015Review
- Dynamic loading and redistribution of the Mcm2-7 helicase complex through the cell cycle.The EMBO journal · 2015Article
- Regulating DNA replication in eukarya.Cold Spring Harbor perspectives in biology · 2013Review
- Genomic instability in cancer.Cold Spring Harbor perspectives in biology · 2013Review
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The replication initiation protein Cdc6p forms a tight complex with Cdc28p, specifically with forms of the kinase that are competent to promote replication initiation. We now show that potential sites of Cdc28 phosphorylation in Cdc6p are required for the regulated destruction of Cdc6p that has been shown to occur during the Saccharomyces cerevisiae cell cycle. Analysis of Cdc6p phosphorylation site mutants and of the requirement for Cdc28p in an in vitro ubiquitination system suggests that targeting of Cdc6p for degradation is more complex than previously proposed. First, phosphorylation of N-terminal sites targets Cdc6p for polyubiquitination probably, as expected, through promoting interaction with Cdc4p, an F box protein involved in substrate recognition by the Skp1-Cdc53-F-box protein (SCF) ubiquitin ligase. However, in addition, mutation of a single, C-terminal site stabilizes Cdc6p in G2 phase cells without affecting substrate recognition by SCF in vitro, demonstrating a second and novel requirement for specific phosphorylation in degradation of Cdc6p. SCF-Cdc4p- and N-terminal phosphorylation site-dependent ubiquitination appears to be mediated preferentially by Clbp/Cdc28p complexes rather than by Clnp/Cdc28ps, suggesting a way in which phosphorylation of Cdc6p might control the timing of its degradation at then end of G1 phase of the cell cycle. The stable cdc6 mutants show no apparent replication defects in wild-type strains. However, stabilization through mutation of three N-terminal phosphorylation sites or of the single C-terminal phosphorylation site leads to dominant lethality when combined with certain mutations in the anaphase-promoting complex.
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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.