Document Detail


Signaling network crosstalk in human pluripotent cells: a Smad2/3-regulated switch that controls the balance between self-renewal and differentiation.
MedLine Citation:
PMID:  22385658     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A general mechanism for how intracellular signaling pathways in human pluripotent cells are coordinated and how they maintain self-renewal remain to be elucidated. In this report, we describe a signaling mechanism where PI3K/Akt activity maintains self-renewal by restraining prodifferentiation signaling through suppression of the Raf/Mek/Erk and canonical Wnt signaling pathways. When active, PI3K/Akt establishes conditions where Activin A/Smad2,3 performs a pro-self-renewal function by activating target genes, including Nanog. When PI3K/Akt signaling is low, Wnt effectors are activated and function in conjunction with Smad2,3 to promote differentiation. The switch in Smad2,3 activity after inactivation of PI3K/Akt requires the activation of canonical Wnt signaling by Erk, which targets Gsk3β. In sum, we define a signaling framework that converges on Smad2,3 and determines its ability to regulate the balance between alternative cell states. This signaling paradigm has far-reaching implications for cell fate decisions during early embryonic development.
Authors:
Amar M Singh; David Reynolds; Timothy Cliff; Satoshi Ohtsuka; Alexa L Mattheyses; Yuhua Sun; Laura Menendez; Michael Kulik; Stephen Dalton
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Cell stem cell     Volume:  10     ISSN:  1875-9777     ISO Abbreviation:  Cell Stem Cell     Publication Date:  2012 Mar 
Date Detail:
Created Date:  2012-03-05     Completed Date:  2012-08-03     Revised Date:  2013-05-20    
Medline Journal Info:
Nlm Unique ID:  101311472     Medline TA:  Cell Stem Cell     Country:  United States    
Other Details:
Languages:  eng     Pagination:  312-26     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier Inc. All rights reserved.
Affiliation:
Department of Biochemistry and Molecular Biology, Paul D. Coverdell Center for Biomedical and Health Sciences, The University of Georgia, Athens, GA 30602, USA.
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MeSH Terms
Descriptor/Qualifier:
Cell Differentiation*
Cells, Cultured
Genes, Switch / physiology*
Humans
Immunoblotting
Models, Biological
Pluripotent Stem Cells / physiology*
Polymerase Chain Reaction
Regeneration*
Signal Transduction*
Smad2 Protein / metabolism,  physiology*
Smad3 Protein / metabolism,  physiology*
Grant Support
ID/Acronym/Agency:
GM75334/GM/NIGMS NIH HHS; HD049647/HD/NICHD NIH HHS; P01 GM085354-01/GM/NIGMS NIH HHS; P01 GM085354-02/GM/NIGMS NIH HHS; P01 GM085354-02S1/GM/NIGMS NIH HHS; P01 GM085354-03/GM/NIGMS NIH HHS; P01 GM085354-04/GM/NIGMS NIH HHS; P01 GM085354-05/GM/NIGMS NIH HHS; R01 HD049647-01A1/HD/NICHD NIH HHS; R01 HD049647-02/HD/NICHD NIH HHS; R01 HD049647-03/HD/NICHD NIH HHS; R01 HD049647-04/HD/NICHD NIH HHS; R01 HD049647-05/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/SMAD2 protein, human; 0/Smad2 Protein; 0/Smad3 Protein
Comments/Corrections
Comment In:
Cell Stem Cell. 2012 Mar 2;10(3):231-2   [PMID:  22385648 ]

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


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