Gill Center for Biomolecular Research, Indiana University, Bloomington, IN 47405.
Department of Neuroscience, University of Austin Texas, Austin, TX 78712.
G3 (Bethesda). 2020 Dec 3;10(12):4425-4438. doi: 10.1534/g3.120.401767.
Nociceptive neurons of larvae are characterized by highly branched dendritic processes whose proper morphogenesis relies on a large number of RNA-binding proteins. Post-transcriptional regulation of RNA in these dendrites has been found to play an important role in their function. Here, we investigate the neuronal functions of two putative RNA modification genes, and , which are predicted to encode pseudouridine synthases. is specifically expressed in larval sensory neurons while expression is ubiquitous. Nociceptor-specific RNAi knockdown of caused hypersensitive nociception phenotypes, which were recapitulated with genetic null alleles. These were rescued with genomic duplication and nociceptor-specific expression of As with , loss of function mutants also displayed hyperalgesia. Interestingly, nociceptor neuron dendrites showed a hyperbranched morphology in the mutants. The latter may be a cause or a consequence of heightened sensitivity in mutant nociception behaviors.
幼虫的伤害感受神经元的特征是具有高度分支的树突状突起，其适当的形态发生依赖于大量的 RNA 结合蛋白。已经发现这些树突中的 RNA 的转录后调控在其功能中起着重要作用。在这里，我们研究了两个假定的 RNA 修饰基因 和 的神经元功能，它们被预测编码假尿嘧啶合酶。 在幼虫感觉神经元中特异性表达，而 表达是普遍存在的。伤害感受神经元特异性 RNAi 敲低 导致超敏伤害感受表型，这些表型可以通过遗传缺失等位基因来重现。这些表型可以通过基因组重复和 在伤害感受神经元中的特异性表达来挽救。与 一样， 功能丧失突变体也表现出痛觉过敏。有趣的是， 突变体中的伤害感受神经元树突显示出超分支的形态。后者可能是突变体伤害感受行为中敏感性增加的原因或结果。
