Studies on developmental mechanisms of the Drosophila visual center

在果蝇中，光感受器细胞在地形图上将它们的轴突发送到第一个视神经节，即视神经板。1.DPP在层状靶区的边缘表达，这里是胶质前体的所在地。抑制该区域的DPP信号导致层状胶质细胞分化缺陷。胶质细胞缺失（gcm）的表达依赖于DPP。此外，显性阴性gcm的表达会损害R轴突的突起和层状胶质细胞的发育，这表明gcm控制着层状胶质细胞的分化。这些结果表明，DPP信号通过控制gcm的表达介导了正确的R轴突投射模式所需的层状胶质细胞的成熟。2.R轴突通过传递诱导信号Hedgehog（Hh）触发层状神经元的增殖和分化。我们发现bHLH-PAS转录因子Single-minded （Sim）是由Hh在层状神经元中诱导的，并且是层状神经元与R轴突关联所必需的。在sim突变的大脑中，层状神经元不能与R轴突结合。因此，层状神经元与R轴突分开。这些数据揭示了轴突和神经元细胞体之间相互作用的一种新的调节机制，这种机制建立了精确的神经元网络。3. 在DWnt4突变体中，视网膜腹侧轴突错误地投射到背层。DWnt4通常在发育层的腹侧表达，沿视网膜腹侧轴突检测到DWnt4蛋白。dzzzzled2和disheveled分别编码Wnt信号传递所需的受体和信号分子。这两个基因的突变引起了DWnt4样缺陷，并且在视网膜中是自主需要的，这表明DWnt4在视网膜轴突引导中的直接作用。相比之下，易洛魁人的同源盒基因是视网膜的背侧线索。

In Drosophila, photoreceptor cells topographically send their axons to the first optic ganglion, the lamina. 1.dpp is expressed at the margin of the lamina target region, where glial precursors reside. Inhibition of DPP signaling in this region resulted in defects in the differentiation of the lamina glial cells. Expression of glial cells missing (gcm) depends on DPP. In addition, R axon projections and lamina glia development were impaired by the expression of a dominant-negative form of gcm, suggesting that gcm controls the differentiation of lamina glial cells. These results suggest that DPP signaling mediates the maturation of the lamina glia required for the correct R axon projection pattern by controlling the expression of gcm. 2.R axons trigger proliferation and differentiation of lamina neurons by delivering the inductive signal, Hedgehog(Hh). We found that the bHLH-PAS transcription factor Single-minded (Sim) is induced by Hh in the lamina neurons and is required for the association of lamina neurons with R axons. In sim mutant brains, lamina neurons fail to associate with R axons. As a result, lamina neurons are set aside from R axons. The data reveal a novel mechanism for regulation of the interaction between axons and neuronal cell bodies that establishes precise neuronal networks. 3. In DWnt4 mutants, ventral retinal axons misprojected to the dorsal lamina. DWnt4 is normally expressed in the ventral half of the developing lamina and DWnt4 protein was detected along ventral retinal axons. Dfrizzled2 and dishevelled, respectively, encode a receptor and a signaling molecule required for Wnt signaling. Mutations in both genes caused DWnt4-like defects, and were autonomously required in the retina, suggesting direct roles of DWnt4 for retinal axon guidance. In contrast, iroquois homeobox genes are the dorsal cues for the retina.