ArticleOpen biology2011
Cell cycle commitment in budding yeast emerges from the cooperation of multiple bistable switches.
Article in Open biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Modeling the START transition in the budding yeast cell cycle.PLoS computational biology · 2024Article
- Data integration strategies for whole-cell modeling.FEMS yeast research · 2024Review
- Editorial: Network-based mathematical modeling in cell and developmental biology.Frontiers in cell and developmental biology · 2024Article
- Cell cycle-independent integration of stress signals by Xbp1 promotes Non-G1/G0 quiescence entry.The Journal of cell biology · 2022Article
- Identifying robust hysteresis in networks.PLoS computational biology · 2018Article
- Experimental testing of a new integrated model of the budding yeast Start transition.Molecular biology of the cell · 2015Article
- A Dynamic Gene Regulatory Network Model That Recovers the Cyclic Behavior of Arabidopsis thaliana Cell Cycle.PLoS computational biology · 2015Article
- Bistability, oscillations, and traveling waves in frog egg extracts.Bulletin of mathematical biology · 2015Article
- Identification of the molecular mechanisms for cell-fate selection in budding yeast through mathematical modeling.Biophysical journal · 2013Article
- Bottom-up construction of in vitro switchable memories.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Double-negative feedback between S-phase cyclin-CDK and CKI generates abruptness in the G1/S switch.Frontiers in physiology · 2012Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The start-transition (START) in the G1 phase marks the point in the cell cycle at which a yeast cell initiates a new round of cell division. Once made, this decision is irreversible and the cell is committed to progressing through the entire cell cycle, irrespective of arrest signals such as pheromone. How commitment emerges from the underlying molecular interaction network is poorly understood. Here, we perform a dynamical systems analysis of an established cell cycle model, which has never been analysed from a commitment perspective. We show that the irreversibility of the START transition and subsequent commitment can be consistently explained in terms of the interplay of multiple bistable molecular switches. By applying an existing mathematical model to a novel problem and by expanding the model in a self-consistent manner, we achieve several goals: we bring together a large number of experimental findings into a coherent theoretical framework; we increase the scope and the applicability of the original model; we give a systems level explanation of how the START transition and the cell cycle commitment arise from the dynamical features of the underlying molecular interaction network; and we make clear, experimentally testable predictions.
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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.