Repression of Fgf signaling by sprouty1-2 regulates cortical patterning in two distinct regions and times.

Repression of Fgf signaling by sprouty1-2 regulates cortical patterning in two distinct regions and times.
复制标题

DOI:
10.1523/jneurosci.0307-10.2010
复制
发表时间:
2010-03-17
期刊:
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子:
--
通讯作者:
Rubenstein JL
Rubenstein JL
中科院分区:
其他
文献类型:
--
作者:
Faedo A;Borello U;Rubenstein JL

文献摘要

被引文献

相似文献

发育生物学的一个基本问题是信号通路如何建立控制细胞增殖、区域命运和细胞命运的转录因子代码。吻侧端脑的形态发生部分受来自吻侧模式中枢(RPC)的fgf信号控制。Fgf信号是如何在脑端调控的对于理解大脑皮层的形成是至关重要的。本研究表明,小鼠Sprouty1和Sprouty2 (Spry1-2)编码Fgf信号的负反馈调节因子,影响皮层的增殖、分化和心室区调节祖细胞身份的基因表达。此外,Spry2在中期神经发生时还具有调控MAPK通路、皮质细胞增殖和基因表达的功能。最后,我们提供的证据表明,Coup-TFI是一种促进尾端命运的转录因子,通过抑制fgf信号传导,部分通过促进Spry表达来实现。
A fundamental question in developmental biology is how signaling pathways establish a transcription factor code that controls cell proliferation, regional fate and cell fate. Morphogenesis of the rostral telencephalon is controlled in part by Fgf-signaling from the rostral patterning center (RPC). How Fgf signaling is regulated in the telencephalon is critical for understanding cerebral cortex formation. Here we show that mouse Sprouty1 and Sprouty2 (Spry1-2), which encode negative feedback regulators of Fgf signaling, are affecting cortical proliferation, differentiation, and the expression of genes regulating progenitor identity in the ventricular zone. In addition, Spry2 has a later function in regulating the MAPK pathway, proliferation and gene expression in the cortex at mid-neurogenesis. Finally, we provide evidence that Coup-TFI, a transcription factor that promotes caudal fate, does so through repressing Fgf-signaling, in part by promoting Spry expression.