Lassiter Rhonda N T, Reynolds Stephanie B, Marin Kristopher D, Mayo Tyler F, Stark Michael R
Department of Physiology and Developmental Biology, Brigham Young University, Provo, Utah 84602, USA.
Dev Dyn. 2009 May;238(5):1073-82. doi: 10.1002/dvdy.21949.
The ophthalmic trigeminal (opV) placode gives rise exclusively to sensory neurons of the peripheral nervous system, providing an advantageous model for understanding neurogenesis. The signaling pathways governing opV placode development have only recently begun to be elucidated. Here, we investigate the fibroblast growth factor receptor-4 (FGFR4), an opV expressed gene, to examine if and how FGF signaling regulates opV placode development. After inhibiting FGFR4, Pax3+ opV placode cells failed to delaminate from the ectoderm and did not contribute to the opV ganglion. Blocking FGF signaling also led to a loss of the early and late neuronal differentiation markers Ngn2, Islet-1, NeuN, and Neurofilament. In addition, without FGF signaling, cells that stalled in the ectoderm lost their opV placode-specific identity by down-regulating Pax3. We conclude that FGF signaling, through FGFR4, is necessary for delamination and differentiation of opV placode cells.
眼三叉神经（opV）基板仅产生周围神经系统的感觉神经元，为理解神经发生提供了一个有利的模型。控制opV基板发育的信号通路直到最近才开始被阐明。在这里，我们研究成纤维细胞生长因子受体4（FGFR4），一个在opV中表达的基因，以检查FGF信号是否以及如何调节opV基板发育。抑制FGFR4后，Pax3+ opV基板细胞无法从外胚层分层，也无法形成opV神经节。阻断FGF信号还导致早期和晚期神经元分化标志物Ngn2、Islet-1、NeuN和神经丝的丢失。此外，在没有FGF信号的情况下，停滞在外胚层的细胞通过下调Pax3失去了opV基板特异性身份。我们得出结论，通过FGFR4的FGF信号对于opV基板细胞的分层和分化是必要的。
