ArticleJournal of the Royal Society, Interface2016
Dissecting mechanisms of mouse embryonic stem cells heterogeneity through a model-based analysis of transcription factor dynamics.
Article in Journal of the Royal Society, Interface, 2016. 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.
- Capturing Pluripotency and Beyond.Cells · 2021Review
- Nuclear gene proximity and protein interactions shape transcript covariations in mammalian single cells.Nature communications · 2020Article
- Agent-based modeling of morphogenetic systems: Advantages and challenges.PLoS computational biology · 2019Review
- Programming Morphogenesis through Systems and Synthetic Biology.Trends in biotechnology · 2018Review
- A stochastic and dynamical view of pluripotency in mouse embryonic stem cells.PLoS computational biology · 2018Article
- Network Features and Dynamical Landscape of Naive and Primed Pluripotency.Biophysical journal · 2018Article
- Article
- Formative pluripotency: the executive phase in a developmental continuum.Development (Cambridge, England) · 2017Review
- An extended model for culture-dependent heterogenous gene expression and proliferation dynamics in mouse embryonic stem cells.NPJ systems biology and applications · 2017Article
- Nanog Dynamics in Mouse Embryonic Stem Cells: Results from Systems Biology Approaches.Stem cells international · 2017Review
- Challenges in long-term imaging and quantification of single-cell dynamics.Nature biotechnology · 2016Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pluripotent mouse embryonic stem cells (mESCs) show heterogeneous expression levels of transcription factors (TFs) involved in pluripotency regulation, among them Nanog and Rex1. The expression of both TFs can change dynamically between states of high and low activity, correlating with the cells' capacity for self-renewal. Stochastic fluctuations as well as sustained oscillations in gene expression are possible mechanisms to explain this behaviour, but the lack of suitable data hampered their clear distinction. Here, we present a systems biology approach in which novel experimental data on TF heterogeneity is complemented by an agent-based model of mESC self-renewal. Because the model accounts for intracellular interactions, cell divisions and heredity structures, it allows for evaluating the consistency of the proposed mechanisms with data on population growth and on TF dynamics after cell sorting. Our model-based analysis revealed that a bistable, noise-driven network model fulfils the minimal requirements to consistently explain Nanog and Rex1 expression dynamics in heterogeneous and sorted mESC populations. Moreover, we studied the impact of TF-related proliferation capacities on the frequency of state transitions and demonstrate that cellular genealogies can provide insights into the heredity structures of mESCs.
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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.