Document Detail

Nanog is required for primitive endoderm formation through a non-cell autonomous mechanism.
MedLine Citation:
PMID:  20435031     Owner:  NLM     Status:  MEDLINE    
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.
Daniel M Messerschmidt; Rolf Kemler
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-05-12
Journal Detail:
Title:  Developmental biology     Volume:  344     ISSN:  1095-564X     ISO Abbreviation:  Dev. Biol.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-23     Completed Date:  2010-08-10     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0372762     Medline TA:  Dev Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  129-37     Citation Subset:  IM    
Copyright Information:
Copyright (c) 2010 Elsevier Inc. All rights reserved.
Department of Molecular Embryology, Max Planck Institute for Immunobiology, Stuebeweg 51, 79108 Freiburg, Germany.
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MeSH Terms
Blastocyst / cytology,  metabolism
Cell Differentiation
Cell Lineage
Endoderm / metabolism*
Gene Expression Regulation, Developmental*
Homeodomain Proteins / metabolism*
Mice, Inbred C57BL
Models, Biological
Time Factors
Transcription Factors / metabolism
Reg. No./Substance:
0/Homeodomain Proteins; 0/Nanog protein, mouse; 0/Transcription Factors

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