ArticlePLoS biology2017
Four simple rules that are sufficient to generate the mammalian blastocyst.
Article in PLoS biology, 2017. 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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Who cites it
29 citing papers in PubMed, 71 citations in OpenAlex.
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- Generative model for the first cell fate bifurcation in mammalian development.Development (Cambridge, England) · 2025Article
- Donor embryonic stem cells displace host cells of 8-cell-stage chimeras to the extra-embryonic lineages by spatial crowding and FGF4 signalling.Development (Cambridge, England) · 2025Article
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- AI-powered simulation-based inference of a genuinely spatial-stochastic gene regulation model of early mouse embryogenesis.PLoS computational biology · 2024Article
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- A geometrical model of cell fate specification in the mouse blastocyst.Development (Cambridge, England) · 2024Article
- Effective mechanical potential of cell-cell interaction in tissues harboring cavity and in cell sheet toward morphogenesis.Frontiers in cell and developmental biology · 2024Article
- Contributions of cell behavior to geometric order in embryonic cartilage.PLoS computational biology · 2023Article
- Lineage tracing identifies heterogeneous hepatoblast contribution to cell lineages and postembryonic organ growth dynamics.PLoS biology · 2023Article
- Adjusting the range of cell-cell communication enables fine-tuning of cell fate patterns from checkerboard to engulfing.Journal of mathematical biology · 2023Article
- Effective mechanical potential of cell-cell interaction explains three-dimensional morphologies during early embryogenesis.PLoS computational biology · 2023Article
- Biophysical models of early mammalian embryogenesis.Stem cell reports · 2023Review
- Seven challenges in the multiscale modeling of multicellular tissues.WIREs mechanisms of disease · 2022Review
- The effects of embryo splitting onIranian journal of veterinary research · 2022Article
- Human embryo polarization requires PLC signaling to mediate trophectoderm specification.eLife · 2021Article
- A multiscale model via single-cell transcriptomics reveals robust patterning mechanisms during early mammalian embryo development.PLoS computational biology · 2021Article
- Cell fate clusters in ICM organoids arise from cell fate heredity and division: a modelling approach.Scientific reports · 2020Article
- Coordination between patterning and morphogenesis ensures robustness during mouse development.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Early mammalian development is both highly regulative and self-organizing. It involves the interplay of cell position, predetermined gene regulatory networks, and environmental interactions to generate the physical arrangement of the blastocyst with precise timing. However, this process occurs in the absence of maternal information and in the presence of transcriptional stochasticity. How does the preimplantation embryo ensure robust, reproducible development in this context? It utilizes a versatile toolbox that includes complex intracellular networks coupled to cell-cell communication, segregation by differential adhesion, and apoptosis. Here, we ask whether a minimal set of developmental rules based on this toolbox is sufficient for successful blastocyst development, and to what extent these rules can explain mutant and experimental phenotypes. We implemented experimentally reported mechanisms for polarity, cell-cell signaling, adhesion, and apoptosis as a set of developmental rules in an agent-based in silico model of physically interacting cells. We find that this model quantitatively reproduces specific mutant phenotypes and provides an explanation for the emergence of heterogeneity without requiring any initial transcriptional variation. It also suggests that a fixed time point for the cells' competence of fibroblast growth factor (FGF)/extracellular signal-regulated kinase (ERK) sets an embryonic clock that enables certain scaling phenomena, a concept that we evaluate quantitatively by manipulating embryos in vitro. Based on these observations, we conclude that the minimal set of rules enables the embryo to experiment with stochastic gene expression and could provide the robustness necessary for the evolutionary diversification of the preimplantation gene regulatory network.
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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.