Document Detail


Functional intestinal stem cells after Paneth cell ablation induced by the loss of transcription factor Math1 (Atoh1).
MedLine Citation:
PMID:  22586121     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Intestinal epithelium has the capacity to self-renew and generate differentiated cells through the existence of two types of epithelial stem cells: active crypt base columnar cells (CBCs) and quiescent +4 cells. The behaviors of these cells are regulated both by intrinsic programs and by extrinsic signals sent by neighboring cells, which define the niche. It is clear that the β-catenin pathway acts as an essential intrinsic signal for the maintenance and proliferation of CBC, and it was recently proposed that Paneth cells provide a crucial niche by secreting Wingless/Int (Wnt) ligands. Here, we examined the effect of disrupting the intestinal stem cell niche by inducible deletion of the transcription factor Math1 (Atoh1), an essential driver of secretory cell differentiation. We found that complete loss of Paneth cells attributable to Math1 deficiency did not perturb the crypt architecture and allowed the maintenance and proliferation of CBCs. Indeed, Math1-deficient crypt cells tolerated in vivo Paneth cell loss and maintained active β-catenin signaling but could not grow ex vivo without exogenous Wnt, implying that, in vivo, underlying mucosal cells act as potential niche. Upon irradiation, Math1-deficient crypt cells regenerated and CBCs continued cycling. Finally, CBC stem cells deficient in adenomatous polyposis coli (Apc) and Math1 were able to promote intestinal tumorigenesis. We conclude that in vivo, Math1-deficient crypts counteract the absence of Paneth cell-derived Wnts and prevent CBC stem cell exhaustion.
Authors:
Aurélie Durand; Bridgitte Donahue; Grégory Peignon; Franck Letourneur; Nicolas Cagnard; Christian Slomianny; Christine Perret; Noah F Shroyer; Béatrice Romagnolo
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-05-14
Journal Detail:
Title:  Proceedings of the National Academy of Sciences of the United States of America     Volume:  109     ISSN:  1091-6490     ISO Abbreviation:  Proc. Natl. Acad. Sci. U.S.A.     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-06-06     Completed Date:  2012-08-27     Revised Date:  2013-05-09    
Medline Journal Info:
Nlm Unique ID:  7505876     Medline TA:  Proc Natl Acad Sci U S A     Country:  United States    
Other Details:
Languages:  eng     Pagination:  8965-70     Citation Subset:  IM    
Affiliation:
Institut Cochin, Department of Endocrinology, Metabolism and Cancer, Université Paris Descartes, Centre National de la Recherche Scientifique Unité Mixte de Recherche 8104, 75014 Paris, France.
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MeSH Terms
Descriptor/Qualifier:
Animals
Basic Helix-Loop-Helix Transcription Factors / deficiency*
Immunohistochemistry
In Situ Hybridization
Intestinal Mucosa / cytology*
Mice
Microarray Analysis
Microscopy, Electron
Paneth Cells / cytology*
Polymerase Chain Reaction
Signal Transduction / physiology*
Stem Cells / ultrastructure*
Wnt Proteins / deficiency
beta Catenin / metabolism*
Grant Support
ID/Acronym/Agency:
CA142826/CA/NCI NIH HHS; R01 CA142826/CA/NCI NIH HHS; R01 DK092306/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Atoh1 protein, mouse; 0/Basic Helix-Loop-Helix Transcription Factors; 0/Wnt Proteins; 0/beta Catenin
Comments/Corrections

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