Yoshida Shoko, Soustelle Laurent, Giangrande Angela, Umetsu Daiki, Murakami Satoshi, Yasugi Tetsuo, Awasaki Takeshi, Ito Kei, Sato Makoto, Tabata Tetsuya
Laboratory of Pattern Formation, Institute of Molecular and Cellular Biosciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-Ku, Tokyo 113-0032, Japan.
Development. 2005 Oct;132(20):4587-98. doi: 10.1242/dev.02040. Epub 2005 Sep 21.
The Drosophila visual system consists of the compound eyes and the optic ganglia in the brain. Among the eight photoreceptor (R) neurons, axons from the R1-R6 neurons stop between two layers of glial cells in the lamina, the most superficial ganglion in the optic lobe. Although it has been suggested that the lamina glia serve as intermediate targets of R axons, little is known about the mechanisms by which these cells develop. We show that DPP signaling plays a key role in this process. dpp is expressed at the margin of the lamina target region, where glial precursors reside. The generation of clones mutant for Medea, the DPP signal transducer, or inhibition of DPP signaling in this region resulted in defects in R neuron projection patterns and in the lamina morphology, which was caused by defects in the differentiation of the lamina glial cells. glial cells missing/glial cells deficient (gcm; also known as glide) is expressed shortly after glia precursors start to differentiate and migrate. Its expression depends on DPP; gcm is reduced or absent in dpp mutants or Medea clones, and ectopic activation of DPP signaling induces ectopic expression of gcm and REPO. In addition, R axon projections and lamina glia development were impaired by the expression of a dominant-negative form of gcm, suggesting that gcm indeed 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.
果蝇视觉系统由复眼和大脑中的视神经节组成。在八个光感受器(R)神经元中,R1 - R6神经元的轴突在视叶最表层神经节——外网层中两层神经胶质细胞之间终止。尽管有人提出外网层神经胶质细胞是R轴突的中间靶标,但对于这些细胞的发育机制却知之甚少。我们发现DPP信号在此过程中起关键作用。dpp在外网层靶区边缘表达,神经胶质前体细胞就位于此处。对DPP信号转导子Medea进行克隆突变,或在此区域抑制DPP信号,都会导致R神经元投射模式和外网层形态出现缺陷,这是由外网层神经胶质细胞分化缺陷引起的。神经胶质细胞缺失/神经胶质细胞缺陷(gcm;也称为glide)在神经胶质前体细胞开始分化和迁移后不久就开始表达。其表达依赖于DPP;在dpp突变体或Medea克隆中,gcm表达减少或缺失,而DPP信号的异位激活会诱导gcm和REPO的异位表达。此外,gcm显性负性形式的表达会损害R轴突投射和外网层神经胶质细胞的发育,这表明gcm确实控制着外网层神经胶质细胞的分化。这些结果表明,DPP信号通过控制gcm的表达来介导正确的R轴突投射模式所需的外网层神经胶质细胞的成熟。