Hey2 regulation by FGF provides a Notch-independent mechanism for maintaining pillar cell fate in the organ of Corti.
Hey2 regulation by FGF provides a Notch-independent mechanism for maintaining pillar cell fate in the organ of Corti.
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DOI：
10.1016/j.devcel.2008.11.008
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发表时间：
2009-01
影响因子：
11.8
通讯作者：
Segil, Neil
中科院分区：
文献类型：
--
作者：
Doetzlhofer, Angelika;Basch, Martin L.;Ohyama, Takahiro;Gessler, Manfred;Groves, Andrew K.;Segil, Neil
Corti器官是内耳的听觉器官，含有两种类型的感觉毛细胞和至少七种支持细胞。这些支持细胞类型大多依赖于Notch依赖的Hes/嘿转录因子的表达来维持支持细胞的命运。在这里，我们证明了Notch信号对支柱细胞命运的分化和维持不是必需的，支柱细胞通过Hey2的表达来区分，并且--不同于其他Hes/嘿因子--Hey2的表达是Notch不依赖的。Hey2被成纤维细胞生长因子激活并阻止毛细胞分化，而Hey2的突变使支柱细胞对Notch信号的丢失敏感，并允许它们分化为毛细胞。我们推测，共同选择的成纤维细胞生长因子信号使Hey2 Notch独立，也将支柱细胞从需要与周围毛细胞直接接触的需要中解放出来，并使内耳复杂的细胞镶嵌的进化重塑成为可能。
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, while 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.
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