%0 Journal Article %1 Doetzlhofer.2009 %A Doetzlhofer, A. %A Basch, M. L. %A Ohyama, T. %A Gessler, M. %A Groves, A. K. %A Segil, N. %D 2009 %J Dev Cell %K *Organ *Receptor;Notch1/genetics/metabolism Amyloid Animals Basic Cell Corti/cytology/physiology Culture Factors/*metabolism Factors/genetics/*metabolism Fibroblast Fusion Growth Helix-Loop-Helix Homeodomain Mice Mice;Knockout Mice;Transgenic Precursor Protein Proteins/genetics/*metabolism Proteins/genetics/metabolism Recombinant Repressor Secretases/antagonists Signal Suppressor Techniques Tissue Transcription Transdifferentiation/physiology Transduction/*physiology Tumor inhibitors of {\&} %N 1 %P 58--69 %T Hey2 regulation by FGF provides a Notch-independent mechanism for maintaining pillar cell fate in the organ of Corti %V 16 %X 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.

@article{Doetzlhofer.2009, 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.}, added-at = {2013-01-29T13:47:26.000+0100}, author = {Doetzlhofer, A. and Basch, M. L. and Ohyama, T. and Gessler, M. and Groves, A. K. and Segil, N.}, biburl = {https://www.bibsonomy.org/bibtex/2343354b5ed32b31e8d8899fbe22f1c6e/ebch}, interhash = {efe8f9e9c98e10e3c7a28d4b1c3dd446}, intrahash = {343354b5ed32b31e8d8899fbe22f1c6e}, journal = {Dev Cell}, keywords = {*Organ *Receptor;Notch1/genetics/metabolism Amyloid Animals Basic Cell Corti/cytology/physiology Culture Factors/*metabolism Factors/genetics/*metabolism Fibroblast Fusion Growth Helix-Loop-Helix Homeodomain Mice Mice;Knockout Mice;Transgenic Precursor Protein Proteins/genetics/*metabolism Proteins/genetics/metabolism Recombinant Repressor Secretases/antagonists Signal Suppressor Techniques Tissue Transcription Transdifferentiation/physiology Transduction/*physiology Tumor inhibitors of {\&}}, number = 1, pages = {58--69}, timestamp = {2013-01-29T13:47:39.000+0100}, title = {Hey2 regulation by FGF provides a Notch-independent mechanism for maintaining pillar cell fate in the organ of Corti}, volume = 16, year = 2009 }