ArticleScientific reports2015
The first two cell-fate decisions of preimplantation mouse embryo development are not functionally independent.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- TEAD4 Regulates apical domain homeostasis and cell-positioning to maintain the trophectoderm lineage during mouse blastocyst development.Open biology · 2026Article
- Immunofluorescence Analysis of Epigenetic Markers in Oocytes and Preimplantation Embryos.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Live imaging endogenous transcription factor dynamics reveals mechanisms of epiblast and primitive endoderm fate segregation.Current biology : CB · 2025Article
- Generative model for the first cell fate bifurcation in mammalian development.Development (Cambridge, England) · 2025Article
- Spatial positioning of preimplantation mouse embryo cells is regulated by mTORC1 and mOpen biology · 2023Article
- Podocalyxin-Like Protein 1 Regulates Pluripotency through the Cholesterol Biosynthesis Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Trophectoderm formation: regulation of morphogenesis and gene expressions by RHO, ROCK, cell polarity, and HIPPO signaling.Reproduction (Cambridge, England) · 2022Review
- Cell size and polarization determine cytokinesis furrow ingression dynamics in mouse embryos.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Cell fate clusters in ICM organoids arise from cell fate heredity and division: a modelling approach.Scientific reports · 2020Article
- The transition from local to global patterns governs the differentiation of mouse blastocysts.PloS one · 2020Article
- Article
- A framework for TRIM21-mediated protein depletion in early mouse embryos: recapitulation of Tead4 null phenotype over three days.BMC genomics · 2019Article
- Similarities and differences in patterns of germline mutation between mice and humans.Nature communications · 2019Article
- Mouse ICM Organoids Reveal Three-Dimensional Cell Fate Clustering.Biophysical journal · 2019Article
- p38-Mitogen Activated Kinases Mediate a Developmental Regulatory Response to Amino Acid Depletion and Associated Oxidative Stress in Mouse Blastocyst Embryos.Frontiers in cell and developmental biology · 2019Article
- HIPPO signaling resolves embryonic cell fate conflicts during establishment of pluripotency in vivo.eLife · 2018Article
- Regulation of energy metabolism during early mammalian development: TEAD4 controls mitochondrial transcription.Development (Cambridge, England) · 2018Article
- Dynamic changes in Sox2 spatio-temporal expression promote the second cell fate decision throughThe Biochemical journal · 2018Article
- The first cell-fate decision of mouse preimplantation embryo development: integrating cell position and polarity.Open biology · 2017Review
- ICM conversion to epiblast by FGF/ERK inhibition is limited in time and requires transcription and protein degradation.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During mouse preimplantation embryo development, three distinct cell lineages are formed, represented by the differentiating trophectoderm (TE), primitive endoderm (PrE) and the pluripotent epiblast (EPI). Classically, lineage derivation has been presented as a two-step process whereby outer TE cells are first segregated from inner-cell mass (ICM), followed by ICM refinement into either the PrE or EPI. As ICM founders can be produced following the fourth or fifth cleavage divisions, their potential to equally contribute to EPI and PrE is contested. Thus, modelling the early sequestration of ICM founders from TE-differentiation after the fourth cleavage division, we examined ICM lineage contribution of varying sized cell clones unable to initiate TE-differentiation. Such TE-inhibited ICM cells do not equally contribute to EPI and PrE and are significantly biased to form EPI. This bias is not caused by enhanced expression of the EPI marker Nanog, nor correlated with reduced apical polarity but associated with reduced expression of PrE-related gene transcripts (Dab2 and Lrp2) and down-regulation of plasma membrane associated Fgfr2. Our results favour a unifying model were the three cell lineages are guided in an integrated, yet flexible, fate decision centred on relative exposure of founder cells to TE-differentiative cues.
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