Sprouty1 and Sprouty2 limit both the size of the otic placode and hindbrain Wnt8a by antagonizing FGF signaling.

Sprouty1 and Sprouty2 limit both the size of the otic placode and hindbrain Wnt8a by antagonizing FGF signaling.
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Sprouty1和Sprouty2通过拮抗FGF信号传导,限制了Otic Placode和后脑WNT8A的大小。

DOI:
10.1016/j.ydbio.2011.02.022
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发表时间:
2011-05-01
影响因子:
2.7
通讯作者:
Shim K
Shim K
中科院分区:
生物学3区
文献类型:
--
作者:
Mahoney Rogers AA;Zhang J;Shim K

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多种信号分子,包括成纤维细胞生长因子 (FGF) 和 Wnt,诱导后脑两侧的两块外胚层形成内耳或耳基板的祖细胞群。在这里,我们报告在 Spry1、Spry2 复合突变体胚胎(Spry1−/−;Spry2−/− 胚胎)中,耳基板的尺寸增加。我们证明,由于通常注定要成为颅表皮的细胞被募集到耳域,耳基板变得更大。 Spry1−/− 中观察到的耳基板增大; Spry2−/− 胚胎先于相邻后脑中 Wnt8a 表达域的扩展。我们证明耳基板的增大和 Wnt8a 表达域的扩展都可以在 Spry1−/− 中得到挽救;通过减少 Fgf10 基因剂量来获得 Spry2−/− 胚胎。我们的结果定义了一个 FGF 响应窗口,在此期间细胞可以不断地募集到耳域,并揭示 SPRY 对假定的 Wnt 诱导中心大小的调节。
Multiple signaling molecules, including Fibroblast Growth Factor (FGF) and Wnt, induce two patches of ectoderm on either side of the hindbrain to form the progenitor cell population for the inner ear, or otic placode. Here we report that in Spry1, Spry2 compound mutant embryos (Spry1−/−; Spry2−/− embryos), the otic placode is increased in size. We demonstrate that the otic placode is larger due to the recruitment of cells, normally destined to become cranial epidermis, into the otic domain. The enlargement of the otic placode observed in Spry1−/−; Spry2−/− embryos is preceded by an expansion of a Wnt8a expression domain in the adjacent hindbrain. We demonstrate that both the enlargement of the otic placode and the expansion of the Wnt8a expression domain can be rescued in Spry1−/−; Spry2−/− embryos by reducing the gene dosage of Fgf10. Our results define a FGF-responsive window during which cells can be continually recruited into the otic domain and uncover SPRY regulation of the size of a putative Wnt inductive center.
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