Specific regions within the embryonic midbrain and cerebellum require different levels of FGF signaling during development.
Specific regions within the embryonic midbrain and cerebellum require different levels of FGF signaling during development.
复制标题
胚胎中脑和小脑内的特定区域需要不同水平的FGF信号传导。
DOI：
10.1242/dev.011569
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发表时间：
2008-03
期刊：
影响因子：
4.6
通讯作者：
Martin, Gail R.
中科院分区：
文献类型：
--
作者：
Basson, M. Albert;Echevarria, Diego;Ahn, Christina Petersen;Sudarov, Anamaria;Joyner, Alexandra L.;Mason, Ivor J.;Martinez, Salvador;Martin, Gail R.
Development of the prospective midbrain and cerebellum are coordinated by FGF ligands produced by the isthmic organizer. Previous studies have suggested that the midbrain and cerebellum require different levels of FGF signaling for their development. However, little is known about the extent to which specific regions within these two parts of the brain differ in their requirement for FGF signaling during embryogenesis. In this study, we have explored the effects of inhibiting FGF signaling within the embryonic midbrain (mesencephalon) and cerebellum (rhombomere 1) by misexpressing Sprouty2 (Spry2) specifically in the mouse mesencephalon and rhombomere 1 from an early stage. We show that such Spry2 misexpression moderately reduces FGF signaling, and that this reduction causes the death of cells in the anterior mesencephalon, the region furthest from the source of FGF ligands. Interestingly, the remaining cells in the posterior mesencephalon develop into anterior midbrain, indicating that a low level of FGF signaling is sufficient to promote only anterior midbrain development. Spry2 misexpression also affects development of the vermis, the medial part of the cerebellum that spans the midline. We found that whereas misexpression of Spry2 alone caused loss of the anterior vermis, reducing FGF signaling further, by decreasing Fgf8 gene dosage, resulted in loss of the entire vermis. We provide evidence that cell death is not responsible for this tissue loss. Instead, our data suggest that the vermis fails to develop because reducing FGF signaling perturbs the balance between vermis and roof plate development in rhombomere 1. We suggest a molecular explanation for this phenomenon by providing evidence that FGF signaling functions to inhibit the BMP signaling that promotes roof plate development.
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