Document Detail


Hey2 regulation by FGF provides a Notch-independent mechanism for maintaining pillar cell fate in the organ of Corti.
MedLine Citation:
PMID:  19154718     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The organ of Corti, the auditory organ of the inner ear, contains two types of sensory hair cells and at least seven types of supporting cells. Most of these supporting cell types rely on Notch-dependent expression of Hes/Hey transcription factors to maintain the supporting cell fate. Here, we show that Notch signaling is not necessary for the differentiation and maintenance of pillar cell fate, that pillar cells are distinguished by Hey2 expression, and that-unlike other Hes/Hey factors-Hey2 expression is Notch independent. Hey2 is activated by FGF and blocks hair cell differentiation, whereas mutation of Hey2 leaves pillar cells sensitive to the loss of Notch signaling and allows them to differentiate as hair cells. We speculate that co-option of FGF signaling to render Hey2 Notch independent also liberated pillar cells from the need for direct contact with surrounding hair cells, and enabled evolutionary remodeling of the complex cellular mosaic of the inner ear.
Authors:
Angelika Doetzlhofer; Martin L Basch; Takahiro Ohyama; Manfred Gessler; Andrew K Groves; Neil Segil
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Developmental cell     Volume:  16     ISSN:  1878-1551     ISO Abbreviation:  Dev. Cell     Publication Date:  2009 Jan 
Date Detail:
Created Date:  2009-01-21     Completed Date:  2009-02-04     Revised Date:  2014-09-14    
Medline Journal Info:
Nlm Unique ID:  101120028     Medline TA:  Dev Cell     Country:  United States    
Other Details:
Languages:  eng     Pagination:  58-69     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Amyloid Precursor Protein Secretases / antagonists & inhibitors
Animals
Basic Helix-Loop-Helix Transcription Factors / genetics,  metabolism*
Cell Transdifferentiation / physiology
Fibroblast Growth Factors / metabolism*
Homeodomain Proteins / genetics,  metabolism
Mice
Mice, Knockout
Mice, Transgenic
Organ of Corti* / cytology,  physiology
Receptor, Notch1* / genetics,  metabolism
Recombinant Fusion Proteins / genetics,  metabolism
Repressor Proteins / genetics,  metabolism*
Signal Transduction / physiology*
Tissue Culture Techniques
Tumor Suppressor Proteins / genetics,  metabolism
Grant Support
ID/Acronym/Agency:
DC008689/DC/NIDCD NIH HHS; DC04189/DC/NIDCD NIH HHS; DC06185/DC/NIDCD NIH HHS; R01 DC004189/DC/NIDCD NIH HHS; R01 DC004189-07/DC/NIDCD NIH HHS; R01 DC004189-08/DC/NIDCD NIH HHS; R01 DC006185/DC/NIDCD NIH HHS; R01 DC006185-03/DC/NIDCD NIH HHS; R01 DC006185-04/DC/NIDCD NIH HHS; R03 DC008689/DC/NIDCD NIH HHS; R03 DC008689-02/DC/NIDCD NIH HHS
Chemical
Reg. No./Substance:
0/Atoh1 protein, mouse; 0/Basic Helix-Loop-Helix Transcription Factors; 0/Hey2 protein, mouse; 0/Homeodomain Proteins; 0/Notch1 protein, mouse; 0/Receptor, Notch1; 0/Recombinant Fusion Proteins; 0/Repressor Proteins; 0/Tumor Suppressor Proteins; 0/prospero-related homeobox 1 protein; 62031-54-3/Fibroblast Growth Factors; EC 3.4.-/Amyloid Precursor Protein Secretases
Comments/Corrections

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


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