FGFs control the patterning of the inner ear but are not able to induce the full ear program
FGFs control the patterning of the inner ear but are not able to induce the full ear program
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DOI：
10.1016/s0925-4773(01)00550-0
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发表时间：
2001-12-01
影响因子：
2.6
通讯作者：
Bober, E
中科院分区：
文献类型：
--
作者：
Adamska, M;Herbrand, H;Bober, E
FGF2 或 FGF8 异位应用，靠近发育中的耳基板，可增强耳标记基因子集（例如 Nkx5-1、SOHol 和 Pax2）的转录。其他 car 表达的基因（Dlx5 和 BMP4）不会被 FGF 上调，异位 FGF 会导致前庭耳蜗神经节的大小增加。这种表型变化是由于上皮细胞向神经元命运的募集增加而不是增殖增强所致。我们还观察到异位 FGF 治疗后会诱导产生额外的囊泡样结构。但这种诱导从未导致全耳项目的注册。我们进一步证明 FGF8 以两个独立的短波表达，首先在耳基板阶段，然后在囊泡阶段。这两种活动都对应于耳朵发育中的关键形态发生事件。我们认为 FGF8 是耳囊模式的重要调节因子。 (C) 2001 Elsevier Science Ireland Ltd. 保留所有权利。
FGF2 or FGF8 applied ectopically, close to the developing otic placode enhances transcription of a subset of ear marker genes such as Nkx5-1, SOHol and Pax2. Other car expressed genes (Dlx5 and BMP4) are not up-regulated by FGFs, Ectopic FGFs lead to an increase in size of the vestibulo-cochlear ganglion. This phenotypic change is due to an increased recruitment of epithelial cells to the neuronal fate rather than to an enhanced proliferation. We also observed an induction of additional, vesicle-like structures upon ectopic FGF treatment. but this induction never led to enrolment of a full ear program. We further demonstrate that FGF8 is expressed in two separate, short waves, first at the otic placode stage and later at the vesicle stage. Both activities correspond to critical morphogenetic events in ear development. We propose that FGF8 is an important regulator of otocyst patterning. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.