ArticleThe Journal of cell biology2013
The spindle checkpoint, APC/C(Cdc20), and APC/C(Cdh1) play distinct roles in connecting mitosis to S phase.
Article in The Journal of cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 58 citations in OpenAlex.
- Regulation of the Cell Cycle by ncRNAs Affects the Efficiency of CDK4/6 Inhibition.International journal of molecular sciences · 2023Review
- Article
- CDC20 in and out of mitosis: a prognostic factor and therapeutic target in hematological malignancies.Journal of experimental & clinical cancer research : CR · 2022Review
- Initial characterization of gap phase introduction in every cell cycle ofFrontiers in cell and developmental biology · 2022Article
- Counting Degrons: Lessons From Multivalent Substrates for Targeted Protein Degradation.Frontiers in physiology · 2022Review
- Understanding the Radiobiology of Vestibular Schwannomas to Overcome Radiation Resistance.Cancers · 2021Review
- Ubiquitin signaling in cell cycle control and tumorigenesis.Cell death and differentiation · 2021Review
- The Insulin Receptor Adaptor IRS2 is an APC/C Substrate That Promotes Cell Cycle Protein Expression and a Robust Spindle Assembly Checkpoint.Molecular & cellular proteomics : MCP · 2020Article
- Ordered dephosphorylation initiated by the selective proteolysis of cyclin B drives mitotic exit.eLife · 2020Article
- AURKA destruction is decoupled from its activity at mitotic exit but is essential to suppress interphase activity.Journal of cell science · 2020Article
- MYCN is amplified during S phase, and c‑myb is involved in controlling MYCN expression and amplification in MYCN‑amplified neuroblastoma cell lines.Molecular medicine reports · 2019Article
- Article
- Accurate delineation of cell cycle phase transitions in living cells with PIP-FUCCI.Cell cycle (Georgetown, Tex.) · 2018Article
- Article
- USP37 deubiquitinates Cdt1 and contributes to regulate DNA replication.Molecular oncology · 2016Article
- PCBP1/HNRNP E1 Protects Chromosomal Integrity by Translational Regulation of CDC27.Molecular cancer research : MCR · 2016Article
- Article
- Feedback regulation between atypical E2Fs and APC/CCdh1 coordinates cell cycle progression.EMBO reports · 2016Article
- Efficient APC/C substrate degradation in cells undergoing mitotic exit depends on K11 ubiquitin linkages.Molecular biology of the cell · 2015Article
- Defective sister chromatid cohesion is synthetically lethal with impaired APC/C function.Nature communications · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA replication depends on a preceding licensing event by Cdt1 and Cdc6. In animal cells, relicensing after S phase but before mitosis is prevented by the Cdt1 inhibitor geminin and mitotic cyclin activity. Here, we show that geminin, like cyclin B1 and securin, is a bona fide target of the spindle checkpoint and APC/C(Cdc20). Cyclin B1 and geminin are degraded simultaneously during metaphase, which directs Cdt1 accumulation on segregating sister chromatids. Subsequent activation of APC/C(Cdh1) leads to degradation of Cdc6 well before Cdt1 becomes unstable in a replication-coupled manner. In mitosis, the spindle checkpoint supports Cdt1 accumulation, which promotes S phase onset. We conclude that the spindle checkpoint, APC/C(Cdc20), and APC/C(Cdh1) act successively to ensure that the disappearance of licensing inhibitors coincides exactly with a peak of Cdt1 and Cdc6. Whereas cell cycle entry from quiescence requires Cdc6 resynthesis, our results indicate that proliferating cells use a window of time in mitosis, before Cdc6 is degraded, as an earlier opportunity to direct S phase.
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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.