Kramer S, West S R, Hiromi Y
Department of Molecular Biology, Princeton University, NJ 08544-1014, USA.
Development. 1995 May;121(5):1361-72. doi: 10.1242/dev.121.5.1361.
Drosophila seven-up is an orphan receptor of the steroid receptor family that is required to specify photoreceptor neuron subtypes in the developing compound eye. Expression of seven-up is confined to four of the eight photoreceptor precursors, R3/R4/R1/R6. We show that misexpression of seven-up in any of the other cell types within the developing ommatidium interferes with their differentiation. Each cell type responds differently to seven-up misexpression. For example, ectopic expression in the non-neuronal cone cells using the sevenless promoter/enhancer (sev-svp) causes the cone cells to take on a neuronal identity. Ectopic expression of seven-up in R2/R5 using the rough enhancer (ro-svp) causes these neurons to lose aspects of their photoreceptor subtype identity while remaining neuronal. Each cell type appears to have a different developmental time window that is sensitive to misexpressed seven-up. The temporal order of responsiveness of each cell type to misexpressed seven-up is similar but not identical to the order of neuronal differentiation. This suggests that there are processes of specification that are distinct from the specification to become a photoreceptor neuron. We have identified members of the ras signaling pathway as suppressors of the cone cell to R7 neuron transformation caused by sev-svp. Suppression of the sev-svp phenotype can be achieved by decreasing the gene-dosage of any of the members of the ras-pathway. This suggests that the function of seven-up in the cone cells requires ras signaling. However, a decrease in ras signaling results in enhancement of the phenotype caused by the ro-svp transgene. We discuss the relationship between decisions controlled by seven-up and those controlled by ras signaling.
果蝇七上蛋白是类固醇受体家族的一个孤儿受体，在发育中的复眼中确定光感受器神经元亚型时是必需的。七上蛋白的表达局限于八个光感受器前体细胞中的四个，即R3/R4/R1/R6。我们发现，在发育中的小眼内的任何其他细胞类型中错误表达七上蛋白会干扰它们的分化。每种细胞类型对七上蛋白错误表达的反应都不同。例如，使用七无启动子/增强子（sev-svp）在非神经元锥形细胞中异位表达会使锥形细胞具有神经元特性。使用粗糙增强子（ro-svp）在R2/R5中异位表达七上蛋白会使这些神经元在保持神经元特性的同时失去其光感受器亚型特性的某些方面。每种细胞类型似乎都有一个对错误表达的七上蛋白敏感的不同发育时间窗口。每种细胞类型对错误表达的七上蛋白的反应时间顺序相似但不完全等同于神经元分化的顺序。这表明存在与成为光感受器神经元的特化过程不同的特化过程。我们已经确定ras信号通路的成员是sev-svp引起的锥形细胞向R7神经元转化的抑制因子。通过降低ras通路任何成员的基因剂量可以实现对sev-svp表型的抑制。这表明七上蛋白在锥形细胞中的功能需要ras信号。然而，ras信号的减少会导致ro-svp转基因引起的表型增强。我们讨论了由七上蛋白控制的决定与由ras信号控制的决定之间的关系。
