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首页> 外文期刊>Developmental biology >The Drosophila IgC2 domain protein Friend-of-Echinoid, a paralogue of Echinoid, limits the number of sensory organ precursors in the wing disc and interacts with the Notch signaling pathway
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The Drosophila IgC2 domain protein Friend-of-Echinoid, a paralogue of Echinoid, limits the number of sensory organ precursors in the wing disc and interacts with the Notch signaling pathway

机译:果蝇IgC2结构域蛋白类铁蛋白的朋友,类铁蛋白的旁系同源物,限制了机翼盘中感觉器官前体的数量,并与Notch信号通路相互作用

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摘要

The Notch signaling pathway is critical in cell fate specification throughout development. In the developing wing disc, single sensory organ precursors (SOPs) are selected from proneural clusters via a process of lateral inhibition mediated by the Notch signaling pathway. The epidermal growth factor receptor (EGFR) pathway has also been implicated in SOP formation. Here, we describe the Drosophila melanogaster gene friend of echinoid (fred), a paralogue of echinoid (ed), a gene recently identified as a negative regulator of the EGFR pathway. fired function was examined in transgenic flies by using inducible RNA interference (RNAi). Suppression of fired in developing wing discs results in specification of ectopic SOPs, additional microchaeta, and cell death. In eye-antennal discs, fired suppression causes a rough eye phenotype. These phenotypes are suppressed by overexpression of Notch, Suppressor of Hairless [Su(H)], and Enhancer of split m7. In contrast, overexpression of Hairless, a negative regulator of the Notch pathway, and decreased Su(H) activity enhance these phenotypes. Thus, fired acts in close concert with the Notch signaling pathway. Dosage-sensitive genetic interaction also suggests a close relationship between fired and ed. [References: 88]
机译:Notch信号通路在整个发育过程中对细胞命运的规范至关重要。在发育中的翼盘中,通过Notch信号通路介导的侧向抑制过程从前神经簇中选择单个感觉器官前体(SOP)。表皮生长因子受体(EGFR)途径也与SOP形成有关。在这里,我们描述了Echinoid(fred)的果蝇果蝇(Drosophila melanogaster)基因朋友,Echinoid(ed)的旁系同源物,该基因最近被鉴定为EGFR通路的负调控因子。使用诱导型RNA干扰(RNAi)检测了转基因果蝇的射击功能。抑制正在发育的机翼盘中的发射会导致异位SOP的规范,额外的微chaeta和细胞死亡。在眼前的椎间盘中,发射抑制会导致粗糙的眼表型。这些表型被Notch的过表达,无毛[Su(H)]的抑制子和m7分裂的增强子所抑制。相反,无毛(Notch途径的负调节剂)的过表达和Su(H)活性的降低增强了这些表型。因此,发射的动作与Notch信号通路密切相关。剂量敏感的遗传相互作用也表明发射和编辑之间存在密切关系。 [参考:88]

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