The establishment of planar cell polarity (PCP) in the Drosophila eye requires correct specification of the R3/R4 pair of photoreceptor cells, determined by a Frizzled mediated signaling event that specifies R3 and induces Delta to activate Notch signaling in the neighboring cell, specifying it as R4. Here, we investigated the role of the Notch signaling negative regulator Numb in the specification of R3/R4 fates and PCP establishment in the Drosophila eye. We observed that Numb is transiently upregulated in R3 at the time of R3/R4 specification. This regulation of Numb levels in developing photoreceptors occurs at the post-transcriptional level and is dependent on Dishevelled, an effector of Frizzled signaling, and Lethal Giant Larva. We detected PCP defects in cells homozygous for numb15, but these defects were due to a loss of function mutation in fat (fatQ805⁎) being present in the numb15 chromosome. However, mosaic overexpression of Numb in R4 precursors (only) caused PCP defects and numb loss-of-function alleles had a modifying effect on the defects found in a hypomorphic dishevelled mutation. Our results suggest that Numb levels are upregulated to reinforce the bias of Notch signaling activation in the R3/R4 pair, two post-mitotic cells that are not specified by asymmetric cell division.

中文翻译：

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果蝇眼中平面细胞极性建立过程中麻木的调节

在果蝇眼中建立平面细胞极性 (PCP) 需要正确指定 R3/R4 对感光细胞，由指定 R3 并诱导 Delta 激活相邻细胞中的 Notch 信号的 Frizzled 介导的信号事件决定，指定它作为 R4。在这里，我们研究了 Notch 信号负调节器 Numb 在果蝇眼中 R3/R4 命运和 PCP 建立的规范中的作用。我们观察到在 R3/R4 规范时，Numb 在 R3 中瞬时上调。这种对发育中的光感受器 Numb 水平的调节发生在转录后水平，并且依赖于 Dishevelled、Frizzled 信号传导的效应器和致命的巨型幼虫。我们在 numb15 纯合细胞中检测到 PCP 缺陷，但这些缺陷是由于 numb15 染色体中存在脂肪（fatQ805⁎）的功能丧失突变所致。然而，R4 前体中 Numb 的镶嵌过度表达（仅）导致 PCP 缺陷，并且麻木功能丧失等位基因对亚形蓬乱突变中发现的缺陷具有修饰作用。我们的结果表明，Numb 水平被上调以加强 R3/R4 对中 Notch 信号激活的偏差，这两个有丝分裂后细胞不是由不对称细胞分裂指定的。