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Plexin A-Semaphorin-1a Reverse Signaling Regulates Photoreceptor Axon Guidance in Drosophila

机译:Plexin A-Semaphorin-1a反向信号调节果蝇中的感光受体轴突指导。

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摘要

While it is well established that Semaphorin family proteins function as axon guidance ligands in invertebrates and vertebrates, several recent studies indicate that the Drosophila Semaphorin-1a (Sema1a), a transmembrane Semaphorin, can also function as a receptor during neural development. The regulator of Sema1a reverse signaling, however, remains unknown. In this study, we show that like Sema1a, the well known Semaphorin receptor Plexin A (PlexA), is required for the proper guidance of photoreceptor (R cell) axons in the Drosophila visual system. Loss of PlexA, like loss of semala, disrupted the association of R-cell growth cones in the optic lobe. Conversely, overexpression of PlexA, like overexpression of sema1a, induced the hyperfasciculation of R-cell axons. Unlike Sema1a, however, the cytoplasmic domain of PlexA is dispensable. Epistasis analysis suggests that PlexA functions upstream of semala. And PlexA and sema1a interact genetically with Rho1. We propose that PlexA regulates Semala reverse signaling in the Drosophila visual system.
机译:尽管已经确定信号蛋白家族蛋白在无脊椎动物和脊椎动物中充当轴突指导配体,但最近的一些研究表明,果蝇Semaphorin-1a(Sema1a)是一种跨膜信号蛋白,在神经发育过程中也可以作为受体。但是,Sema1a反向信号的调节剂仍然未知。在这项研究中,我们显示像Sema1a,众所周知的Semaphorin受体Plexin A(PlexA),是在果蝇视觉系统中正确引导感光细胞(R细胞)轴突所必需的。 PlexA的丢失(如semala的丢失)破坏了视细胞中R细胞生长锥的关联。相反,PlexA的过度表达与sema1a的过度表达一样,会引起R细胞轴突的超束缚。但是,与Sema1a不同,PlexA的胞质结构域是可有可无的。上位性分析表明,PlexA在semala的上游起作用。 PlexA和sema1a与Rho1发生遗传相互作用。我们建议PlexA调节果蝇视觉系统中的Semala反向信号。

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