AP2-dependent signals from the ectoderm regulate craniofacial development in the zebrafish embryo
AP2-dependent signals from the ectoderm regulate craniofacial development in the zebrafish embryo
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DOI：
10.1242/dev.01879
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发表时间：
2005-07-01
期刊：
影响因子：
4.6
通讯作者：
Schilling, TF
中科院分区：
文献类型：
--
作者：
Knight, RD;Javidan, Y;Schilling, TF
AP2转录因子调节胚胎发育的许多方面。在小鼠和斑马鱼中对AP2a（Tfap2a）功能的研究已经证明了在形成颅面骨骼的神经嵴起源的间充质细胞的图案化中的作用，而哺乳动物Tfap2b在面部骨骼和肾脏中都是必需的。在这里，我们展示了斑马鱼tfap2a和tfap2b在面部外胚层发育中的重要功能，以及神经嵴细胞（NCC）中诱导骨骼发生的上皮信号。tfap2a和tfap2b缺陷的斑马鱼胚胎表现出表皮细胞存活缺陷，并且缺乏NCC衍生的软骨。我们发现，软骨缺损后出现NCC迁移在骨骼分化，他们可以通过移植野生型外胚层获救。我们提出了一个模型，其中AP2蛋白在颅NCC中发挥两种不同的作用：早期细胞自主功能的细胞规格和生存，以及后来的非自主功能调节外胚层信号，诱导骨骼生成。
AP2 transcription factors regulate many aspects of embryonic development. Studies of AP2a (Tfap2a) function in mice and zebrafish have demonstrated a role in patterning mesenchymal cells of neural crest origin that form the craniofacial skeleton, while the mammalian Tfap2b is required in both the facial skeleton and kidney. Here, we show essential functions for zebrafish tfap2a and tfap2b in development of the facial ectoderm, and for signals from this epithelium that induce skeletogenesis in neural crest cells (NCCs). Zebrafish embryos deficient for both tfap2a and tfap2b show defects in epidermal cell survival and lack NCC-derived cartilages. We show that cartilage defects arise after NCC migration during skeletal differentiation, and that they can be rescued by transplantation of wild-type ectoderm. We propose a model in which AP2 proteins play two distinct roles in cranial NCCs: an early cell-autonomous function in cell specification and survival, and a later non-autonomous function regulating ectodermal signals that induce skeletogenesis.