Notch-mediated lateral induction is necessary to maintain vestibular prosensory identity during inner ear development

被引:14
作者
Brown, Rogers M., II [1 ]
Nelson, Joel C. [2 ]
Zhang, Hongyuan [3 ]
Kiernan, Amy E. [5 ,6 ]
Groves, Andrew K. [1 ,2 ,3 ,4 ]
机构
[1] Baylor Coll Med, Program Dev Biol, 1 Baylor Plaza, Houston, TX 77030 USA
[2] Baylor Coll Med, Program Integrat Mol & Biomed Sci, 1 Baylor Plaza, Houston, TX 77030 USA
[3] Baylor Coll Med, Dept Neurosci, 1 Baylor Plaza, Houston, TX 77030 USA
[4] Baylor Coll Med, Dept Mol & Human Genet, 1 Baylor Plaza, Houston, TX 77030 USA
[5] Univ Rochester, Dept Ophthalmol, New York, NY 14642 USA
[6] Univ Rochester, Dept Genet, New York, NY 14642 USA
关键词
Notch; Inner ear; Vestibular; Otic; Sensory; Development; CELL FATE; HAIR-CELLS; EXPRESSION PATTERNS; PROGENITOR CELLS; OTIC PLACODE; ORGAN; GENE; GENERATION; EVOLUTION; REVEALS;
D O I
10.1016/j.ydbio.2020.02.015
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
The five vestibular organs of the inner ear derive from patches of prosensory cells that express the transcription factor SOX2 and the Notch ligand JAG1. Previous work suggests that JAG1-mediated Notch signaling is both necessary and sufficient for prosensory formation and that the separation of developing prosensory patches is regulated by LMX1a, which antagonizes Notch signaling. We used an inner ear-specific deletion of the Rbpj kappa gene in which Notch signaling is progressively lost from the inner ear to show that Notch signaling, is continuously required for the maintenance of prosensory fate. Loss of Notch signaling in prosensory patches causes them to shrink and ultimately disappear. We show this loss of prosensory fate is not due to cell death, but rather to the conversion of prosensory tissue into non-sensory tissue that expresses LMX1a. Notch signaling is therefore likely to stabilize, rather than induce prosensory fate.
引用
收藏
页码:74 / 84
页数:11
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