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SIFamide and SIFamide Receptor Define a Novel Neuropeptide Signaling to Promote Sleep in Drosophila

机译:SIFamide和SIFamide受体定义了一种新型的神经肽信号来促进果蝇的睡眠

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摘要

SIFamide receptor (SIFR) is a Drosophila G protein-coupled receptor for the neuropeptide SIFamide (SIFa). Although the sequence and spatial expression of SIFa are evolutionarily conserved among insect species, the physiological function of SIFa/SIFR signaling remains elusive. Here, we provide genetic evidence that SIFa and SIFR promote sleep in Drosophila. Either genetic ablation of SIFa-expressing neurons in the pars intercerebralis (PI) or pan-neuronal depletion of SIFa expression shortened baseline sleep and reduced sleep-bout length, suggesting that it caused sleep fragmentation. Consistently, RNA interference-mediated knockdown of SIFR expression caused short sleep phenotypes as observed in SIFa-ablated or depleted flies. Using a panel of neuron-specific Gal4 drivers, we further mapped SIFR effects to subsets of PI neurons. Taken together, these results reveal a novel physiological role of the neuropeptide SIFa/SIFR pathway to regulate sleep through sleep-promoting neural circuits in the PI of adult fly brains.
机译:SIFamide受体(SIFR)是果蝇G蛋白偶联的神经肽SIFamide(SIFa)受体。尽管SIFa的序列和空间表达在昆虫物种之间在进化上是保守的,但SIFa / SIFR信号转导的生理功能仍然难以捉摸。在这里,我们提供了SIFa和SIFR促进果蝇睡眠的遗传证据。大脑中部脑组织(PI)中表达SIFa的神经元的遗传消融或SIFa表达的泛神经元耗竭会缩短基线睡眠并缩短睡眠周期,这表明这会导致睡眠碎片。一致地,RNA干扰介导的SIFR表达的敲低会导致短暂的睡眠表型,如在SIFa消融或枯竭的果蝇中观察到的。使用一组特定于神经元的Gal4驱动程序,我们进一步将SIFR效应映射到PI神经元的子集。综上所述,这些结果揭示了神经肽SIFa / SIFR途径通过成年果蝇大脑的PI中通过促进睡眠的神经回路调节睡眠的新型生理作用。

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