ArticlePLoS computational biology2015
Cell cycle control by a minimal Cdk network.
Article in PLoS computational biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 59 citations in OpenAlex.
- Decoding Cdk1 control: from mitotic thresholds to meiotic specificity.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2026Review
- Capturing CDKs in action: Live-cell biosensors pioneer the new frontiers in cell cycle research.Cell structure and function · 2025Review
- The bistable mitotic switch in fission yeast.Molecular biology of the cell · 2024Article
- R-loop and diseases: the cell cycle matters.Molecular cancer · 2024Review
- Artificial Modulation and Rewiring of Cell Cycle Progression Using Synthetic Circuits in Fission Yeast.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Time-keeping and decision-making in the cell cycle.Interface focus · 2022Review
- Cyclin/Forkhead-mediated coordination of cyclin waves: an autonomous oscillator rationalizing the quantitative model of Cdk control for budding yeast.NPJ systems biology and applications · 2021Review
- Computational modeling of chromosome re-replication in mutant strains of fission yeast.Molecular biology of the cell · 2021Article
- Adaptive behaviour and learning in slime moulds: the role of oscillations.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2021Article
- The fission yeast S-phase cyclin Cig2 can drive mitosis.Genetics · 2021Article
- Clb3-centered regulations are recurrent across distinct parameter regions in minimal autonomous cell cycle oscillator designs.NPJ systems biology and applications · 2020Article
- Network mechanisms and dysfunction within an integrated computational model of progression through mitosis in the human cell cycle.PLoS computational biology · 2020Article
- Computer-Aided Whole-Cell Design: Taking a Holistic Approach by Integrating Synthetic With Systems Biology.Frontiers in bioengineering and biotechnology · 2020Article
- Noisy Cell-Size-Correlated Expression of Cyclin B Drives Probabilistic Cell-Size Homeostasis in Fission Yeast.Current biology : CB · 2019Article
- A checkpoint-oriented cell cycle simulation model.Cell cycle (Georgetown, Tex.) · 2019Article
- Degradation of cyclin B is critical for nuclear division inBiology open · 2018Article
- Cyclin Y Modulates the Proliferation, Invasion, and Metastasis of Hepatocellular Carcinoma Cells.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Adding phosphorylation events to the core oscillator driving the cell cycle of fission yeast.PloS one · 2018Article
- Clinical role and biological function of CDK5 in hepatocellular carcinoma: A study based on immunohistochemistry, RNA-seq andOncotarget · 2017Article
- Coarse-graining and hybrid methods for efficient simulation of stochastic multi-scale models of tumour growth.Journal of computational physics · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
Abstract
In present-day eukaryotes, the cell division cycle is controlled by a complex network of interacting proteins, including members of the cyclin and cyclin-dependent protein kinase (Cdk) families, and the Anaphase Promoting Complex (APC). Successful progression through the cell cycle depends on precise, temporally ordered regulation of the functions of these proteins. In light of this complexity, it is surprising that in fission yeast, a minimal Cdk network consisting of a single cyclin-Cdk fusion protein can control DNA synthesis and mitosis in a manner that is indistinguishable from wild type. To improve our understanding of the cell cycle regulatory network, we built and analysed a mathematical model of the molecular interactions controlling the G1/S and G2/M transitions in these minimal cells. The model accounts for all observed properties of yeast strains operating with the fusion protein. Importantly, coupling the model's predictions with experimental analysis of alternative minimal cells, we uncover an explanation for the unexpected fact that elimination of inhibitory phosphorylation of Cdk is benign in these strains while it strongly affects normal cells. Furthermore, in the strain without inhibitory phosphorylation of the fusion protein, the distribution of cell size at division is unusually broad, an observation that is accounted for by stochastic simulations of the model. Our approach provides novel insights into the organization and quantitative regulation of wild type cell cycle progression. In particular, it leads us to propose a new mechanistic model for the phenomenon of mitotic catastrophe, relying on a combination of unregulated, multi-cyclin-dependent Cdk activities.
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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.