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PMID:19154718

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Citation

Doetzlhofer, A, Basch, ML, Ohyama, T, Gessler, M, Groves, AK and Segil, N (2009) Hey2 regulation by FGF provides a Notch-independent mechanism for maintaining pillar cell fate in the organ of Corti. Dev. Cell 16:58-69

Abstract

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.

Links

PubMed PMC2696015 Online version:10.1016/j.devcel.2008.11.008

Keywords

Amyloid Precursor Protein Secretases/antagonists & inhibitors; Animals; Basic Helix-Loop-Helix Transcription Factors/genetics; Basic Helix-Loop-Helix Transcription Factors/metabolism; Cell Transdifferentiation/physiology; Fibroblast Growth Factors/metabolism; Homeodomain Proteins/genetics; Homeodomain Proteins/metabolism; Mice; Mice, Knockout; Mice, Transgenic; Organ of Corti/cytology; Organ of Corti/physiology; Receptor, Notch1/genetics; Receptor, Notch1/metabolism; Recombinant Fusion Proteins/genetics; Recombinant Fusion Proteins/metabolism; Repressor Proteins/genetics; Repressor Proteins/metabolism; Signal Transduction/physiology; Tissue Culture Techniques; Tumor Suppressor Proteins/genetics; Tumor Suppressor Proteins/metabolism

Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

MOUSE:SUH

acts_upstream_of_or_within

GO:0007219: Notch signaling pathway

ECO:0000315: mutant phenotype evidence used in manual assertion

MGI:MGI:3046196,MGI:MGI:3583755

P

Seeded From UniProt

complete

MOUSE:SUH

acts_upstream_of_or_within

GO:0009912: auditory receptor cell fate commitment

ECO:0000315: mutant phenotype evidence used in manual assertion

MGI:MGI:3046196,MGI:MGI:3583755

P

  • results_in_commitment_to:(CL:0000589)

Seeded From UniProt

complete

MOUSE:ATOH1

acts_upstream_of_or_within

GO:0045609: positive regulation of inner ear auditory receptor cell differentiation

ECO:0000314: direct assay evidence used in manual assertion

P

  • regulates_o_results_in_acquisition_of_features_of:(CL:0000202)

Seeded From UniProt

complete

MOUSE:NOTC1

acts_upstream_of_or_within

GO:0007219: Notch signaling pathway

ECO:0000315: mutant phenotype evidence used in manual assertion

MGI:MGI:3044585,MGI:MGI:3046196

P

Seeded From UniProt

complete

MOUSE:NOTC1

acts_upstream_of_or_within

GO:0009912: auditory receptor cell fate commitment

ECO:0000315: mutant phenotype evidence used in manual assertion

MGI:MGI:3044585,MGI:MGI:3046196

P

  • results_in_commitment_to:(CL:0000202)

Seeded From UniProt

complete

MOUSE:HEY2

acts_upstream_of_or_within

GO:0045607: regulation of inner ear auditory receptor cell differentiation

ECO:0000316: genetic interaction evidence used in manual assertion

MGI:MGI:104654

P

  • regulates_o_results_in_acquisition_of_features_of:(CL:0000202)

Seeded From UniProt

complete

MOUSE:HEY2

acts_upstream_of_or_within

GO:0045165: cell fate commitment

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete


See also

References

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