Cell fate control in the Drosophila retina by the orphan receptor seven-up: its role in the decisions mediated by the ras signaling pathway.
Cell fate control in the Drosophila retina by the orphan receptor seven-up: its role in the decisions mediated by the ras signaling pathway.
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发表时间：
1995-05
期刊：
影响因子：
4.6
通讯作者：
S. Kramer;S. West;Y. Hiromi
中科院分区：
文献类型：
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作者：
S. Kramer;S. West;Y. Hiromi
果蝇seven-up是类固醇受体家族的孤儿受体，其在发育中的复眼中指定感光神经元亚型所需。七喜的表达仅限于八种感光细胞前体中的四种，R3/R4/R1/R6。我们发现，在发育中的小眼内的任何其他类型的细胞中，七喜的错误表达干扰了它们的分化。每种细胞类型对七喜错误表达的反应不同。例如，使用sevenless启动子/增强子（sevenless promoter/enhancer，sev-svp）在非神经元视锥细胞中的异位表达导致视锥细胞呈现神经元身份。使用粗糙增强子（ro-svp）在R2/R5中异位表达seven-up导致这些神经元在保持神经元的同时失去其感光器亚型身份的方面。每种细胞类型似乎有不同的发育时间窗，对错误表达的七喜敏感。每种细胞类型对错误表达的七喜的反应的时间顺序与神经元分化的顺序相似但不相同。这表明，存在着与成为感光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引起的视锥细胞向R7神经元转化的抑制因子。sev-svp表型的抑制可以通过减少ras途径任何成员的基因剂量来实现。这表明视锥细胞中七喜的功能需要ras信号。然而，ras信号转导的减少导致ro-svp转基因引起的表型增强。我们讨论了七喜控制的决策和ras信号控制的决策之间的关系。
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.