Document Detail


Regulation of extra-embryonic endoderm stem cell differentiation by Nodal and Cripto signaling.
MedLine Citation:
PMID:  21862554     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The signaling pathway for Nodal, a ligand of the TGFβ superfamily, plays a central role in regulating the differentiation and/or maintenance of stem cell types that can be derived from the peri-implantation mouse embryo. Extra-embryonic endoderm stem (XEN) cells resemble the primitive endoderm of the blastocyst, which normally gives rise to the parietal and the visceral endoderm in vivo, but XEN cells do not contribute efficiently to the visceral endoderm in chimeric embryos. We have found that XEN cells treated with Nodal or Cripto (Tdgf1), an EGF-CFC co-receptor for Nodal, display upregulation of markers for visceral endoderm as well as anterior visceral endoderm (AVE), and can contribute to visceral endoderm and AVE in chimeric embryos. In culture, XEN cells do not express Cripto, but do express the related EGF-CFC co-receptor Cryptic (Cfc1), and require Cryptic for Nodal signaling. Notably, the response to Nodal is inhibited by the Alk4/Alk5/Alk7 inhibitor SB431542, but the response to Cripto is unaffected, suggesting that the activity of Cripto is at least partially independent of type I receptor kinase activity. Gene set enrichment analysis of genome-wide expression signatures generated from XEN cells under these treatment conditions confirmed the differing responses of Nodal- and Cripto-treated XEN cells to SB431542. Our findings define distinct pathways for Nodal and Cripto in the differentiation of visceral endoderm and AVE from XEN cells and provide new insights into the specification of these cell types in vivo.
Authors:
Marianna Kruithof-de Julio; Mariano J Alvarez; Antonella Galli; Jianhua Chu; Sandy M Price; Andrea Califano; Michael M Shen
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Development (Cambridge, England)     Volume:  138     ISSN:  1477-9129     ISO Abbreviation:  Development     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-08-24     Completed Date:  2011-11-02     Revised Date:  2012-09-28    
Medline Journal Info:
Nlm Unique ID:  8701744     Medline TA:  Development     Country:  England    
Other Details:
Languages:  eng     Pagination:  3885-95     Citation Subset:  IM    
Affiliation:
Department of Medicine, Columbia University Medical Center, New York, NY 10032, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Differentiation / drug effects,  genetics*
Cell Line
Embryo, Mammalian
Embryonic Stem Cells / drug effects,  metabolism,  physiology*
Endoderm / cytology*,  drug effects,  metabolism,  physiology*
Epidermal Growth Factor / genetics,  metabolism,  pharmacology,  physiology*
Extraembryonic Membranes / cytology,  physiology
Female
Gene Expression Profiling
Membrane Glycoproteins / genetics,  metabolism,  pharmacology,  physiology*
Mice
Mice, Inbred ICR
Mice, Transgenic
Microarray Analysis
Neoplasm Proteins / genetics,  metabolism,  pharmacology,  physiology*
Nodal Protein / genetics,  metabolism,  pharmacology,  physiology*
Pregnancy
Signal Transduction / drug effects,  genetics
Grant Support
ID/Acronym/Agency:
HD42837/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Membrane Glycoproteins; 0/Neoplasm Proteins; 0/Nodal Protein; 0/Nodal protein, mouse; 0/Tdgf1 protein, mouse; 62229-50-9/Epidermal Growth Factor
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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