Studies on developmental mechanisms of the Drosophila visual center

在果蝇中，感光细胞拓扑地将它们的轴突发送到第一个视神经节，即板层。1. DPP在神经胶质前体所在的椎板靶区域的边缘表达。DPP信号在这一地区的抑制导致在板神经胶质细胞的分化缺陷。胶质细胞缺失（gcm）的表达依赖于DPP。此外，R轴突的预测和板层胶质细胞的发展受损的显性负形式的gcm的表达，这表明gcm控制板层胶质细胞的分化。这些结果表明，DPP信号介导的成熟所需的正确的R轴突投射模式的板胶质细胞通过控制gcm的表达。2.R轴突通过传递诱导信号Hedgehog（Hh）触发板层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诱导的，是板层神经元与R轴突联系所必需的。在sim突变的大脑中，板层神经元不能与R轴突联系。因此，板层神经元与R轴突分开。这些数据揭示了一种新的机制，用于调节轴突和神经元细胞体之间的相互作用，建立精确的神经元网络。3.在DWnt 4突变体中，腹侧视网膜轴突错误投射到背侧椎板。DWnt 4通常在发育中的板层的腹侧一半中表达，并且沿着腹侧视网膜轴突检测到DWnt 4蛋白。Dfrizzled 2和disevelled分别编码Wnt信号传导所需的受体和信号分子。这两个基因的突变引起了DWnt 4样缺陷，并且在视网膜中自主需要，这表明DWnt 4对视网膜轴突引导的直接作用。相反，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.