| Nanog is required for primitive endoderm formation through a non-cell autonomous mechanism. | |
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MedLine Citation:
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PMID: 20435031 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Early lineage segregation in mouse development results in two, either CDX2- or OCT4/NANOG-positive, cell populations. CDX2-positive cells form the trophectoderm (TE), OCT4/NANOG-positive cells the inner cell mass (ICM). In a second lineage decision ICM cells segregate into Epiblast (EPI) and primitive endoderm (PE). EPI and PE formation depend on the activity of the transcription factors Nanog and Gata4/6. A role for Nanog, a crucial pluripotency factor, in preventing PE differentiation has been proposed, as outgrowths of mutant ICMs result in PE, but not EPI derivatives. We established Nanog-mutant mouse lines and analyzed EPI and PE formation in vivo. Surprisingly, Gata4 expression in mutant ICM cells is absent or strongly decreased, thus loss of Nanog does not result in precocious endoderm differentiation. However, Nanog-deficient embryos retain the capacity to form PE in chimeric embryos and, in contrast to recent reports, in blastocyst outgrowths. Based on our findings we propose a non-cell autonomous requirement of Nanog for proper PE formation in addition to its essential role in EPI determination. |
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Authors:
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Daniel M Messerschmidt; Rolf Kemler |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-05-12 |
Journal Detail:
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Title: Developmental biology Volume: 344 ISSN: 1095-564X ISO Abbreviation: Dev. Biol. Publication Date: 2010 Aug |
Date Detail:
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Created Date: 2010-07-23 Completed Date: 2010-08-10 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0372762 Medline TA: Dev Biol Country: United States |
Other Details:
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Languages: eng Pagination: 129-37 Citation Subset: IM |
Copyright Information:
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Copyright (c) 2010 Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Molecular Embryology, Max Planck Institute for Immunobiology, Stuebeweg 51, 79108 Freiburg, Germany. daniel.m@imb.a-star.edu.sg |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Alleles Animals Biopsy Blastocyst / cytology, metabolism Cell Differentiation Cell Lineage Endoderm / metabolism* Gene Expression Regulation, Developmental* Genotype Homeodomain Proteins / metabolism* Mice Mice, Inbred C57BL Models, Biological Time Factors Transcription Factors / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Homeodomain Proteins; 0/Nanog protein, mouse; 0/Transcription Factors |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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