ArticleOpen biology2016
p38 (Mapk14/11) occupies a regulatory node governing entry into primitive endoderm differentiation during preimplantation mouse embryo development.
Article in Open biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- The dynamic expression pattern of signaling pathways involved in early embryo development.Cell communication and signaling : CCS · 2026Article
- Wnt/β-catenin signalling modulates the timing of cell fate decision making in the early mouse embryo.PloS one · 2026Article
- Primitive means first, not worst: Critical roles for primitive endoderm in embryos and embryo models.Developmental biology · 2025Review
- The salt-and-pepper pattern in mouse blastocysts is compatible with signaling beyond the nearest neighbors.iScience · 2023Article
- Spatial positioning of preimplantation mouse embryo cells is regulated by mTORC1 and mOpen biology · 2023Article
- Article
- Journey of the mouse primitive endoderm: from specification to maturation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Paracrine interactions through FGFR1 and FGFR2 receptors regulate the development of preimplantation mouse chimaeric embryo.Open biology · 2022Article
- Environmental Exposures around Conception: Developmental Pathways Leading to Lifetime Disease Risk.International journal of environmental research and public health · 2021Review
- DDX21 is a p38-MAPK-sensitive nucleolar protein necessary for mouse preimplantation embryo development and cell-fate specification.Open biology · 2021Article
- Overexpression of miRNA-22-3p attenuates osteoporosis by targeting MAPK14.Experimental and therapeutic medicine · 2021Article
- p38-MAPK-mediated translation regulation during early blastocyst development is required for primitive endoderm differentiation in mice.Communications biology · 2021Article
- Cell fate clusters in ICM organoids arise from cell fate heredity and division: a modelling approach.Scientific reports · 2020Article
- FGF signaling regulates development by processes beyond canonical pathways.Genes & development · 2020Article
- 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
- Dynamic changes in Sox2 spatio-temporal expression promote the second cell fate decision throughThe Biochemical journal · 2018Article
- Plasticity of the inner cell mass in mouse blastocyst is restricted by the activity of FGF/MAPK pathway.Scientific reports · 2017Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During mouse preimplantation embryo development, the classically described second cell-fate decision involves the specification and segregation, in blastocyst inner cell mass (ICM), of primitive endoderm (PrE) from pluripotent epiblast (EPI). The active role of fibroblast growth factor (Fgf) signalling during PrE differentiation, particularly in the context of Erk1/2 pathway activation, is well described. However, we report that p38 family mitogen-activated protein kinases (namely p38α/Mapk14 and p38β/Mapk11; referred to as p38-Mapk14/11) also participate in PrE formation. Specifically, functional p38-Mapk14/11 are required, during early-blastocyst maturation, to assist uncommitted ICM cells, expressing both EPI and earlier PrE markers, to fully commit to PrE differentiation. Moreover, functional activation of p38-Mapk14/11 is, as reported for Erk1/2, under the control of Fgf-receptor signalling, plus active Tak1 kinase (involved in non-canonical bone morphogenetic protein (Bmp)-receptor-mediated PrE differentiation). However, we demonstrate that the critical window of p38-Mapk14/11 activation precedes the E3.75 timepoint (defined by the initiation of the classical 'salt and pepper' expression pattern of mutually exclusive EPI and PrE markers), whereas appropriate lineage maturation is still achievable when Erk1/2 activity (via Mek1/2 inhibition) is limited to a period after E3.75. We propose that active p38-Mapk14/11 act as enablers, and Erk1/2 as drivers, of PrE differentiation during ICM lineage specification and segregation.
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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 Socratic graph.