Park Sangjin, Sonn Jun Young, Oh Yangkyun, Lim Chunghun, Choe Joonho
Department of Biological Sciences, College of Life Science and Bioengineering, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea.
Department of Biological Sciences, School of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan 689-798, Korea.
Mol Cells. 2014 Apr;37(4):295-301. doi: 10.14348/molcells.2014.2371. Epub 2014 Mar 21.
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.
SIF酰胺受体(SIFR)是一种果蝇G蛋白偶联受体,用于神经肽SIF酰胺(SIFa)。尽管SIFa的序列和空间表达在昆虫物种中具有进化保守性,但SIFa/SIFR信号传导的生理功能仍然难以捉摸。在这里,我们提供了遗传学证据,表明SIFa和SIFR促进果蝇睡眠。在脑间部(PI)中对表达SIFa的神经元进行基因消融或全神经元SIFa表达缺失均缩短了基线睡眠并减少了睡眠时长,这表明它导致了睡眠碎片化。一致地,RNA干扰介导的SIFR表达敲低导致了与SIFa消融或缺失果蝇中观察到的短睡眠表型。使用一组神经元特异性Gal4驱动子,我们进一步将SIFR的作用定位到PI神经元的亚群。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PI中的促睡眠神经回路调节睡眠的新生理作用。