Laboratory of Molecular Chronobiology, Douglas Mental Health University Institute, Montréal, Quebec, Canada.
PLoS One. 2011;6(10):e26430. doi: 10.1371/journal.pone.0026430. Epub 2011 Oct 20.
Orexins (OX-A, OX-B) are neuropeptides involved in the regulation of the sleep-wake cycle, feeding and reward, via activation of orexin receptors 1 and 2 (OX1R, OX2R). The loss of orexin peptides or functional OX2R has been shown to cause the sleep disorder, narcolepsy. Since the regulation of orexin receptors remains largely undefined, we searched for novel protein partners of the intracellular tail of orexin receptors. Using a yeast two-hybrid screening strategy in combination with co-immunoprecipitation experiments, we found interactions between OX1R and the dynein light chains Tctex-type 1 and 3 (Dynlt1, Dynlt3). These interactions were mapped to the C-terminal region of the dynein light chains and to specific residues within the last 10 amino acids of OX1R. Hence, we hypothesized that dynein light chains could regulate orexin signaling. In HEK293 cells expressing OX1R, stimulation with OX-A produced a less sustained extracellular signal-regulated kinases 1/2 (ERK1/2) activation when Dynlt1 was co-expressed, while it was prolonged under reduced Dynlt1 expression. The amount of OX1R located at the plasma membrane as well as the kinetics and extent of OX-A-induced internalization of OX1R (disappearance from membrane) were not altered by Dynlt1. However, Dynlt1 reduced the localization of OX1R in early endosomes following initial internalization. Taken together, these data suggest that Dynlt1 modulates orexin signaling by regulating OX1R, namely its intracellular localization following ligand-induced internalization.
食欲素(OX-A、OX-B)是参与调节睡眠-觉醒周期、摄食和奖赏的神经肽,通过激活食欲素受体 1 和 2(OX1R、OX2R)。已经表明,食欲素肽的缺失或功能性 OX2R 的缺失会导致睡眠障碍——发作性睡病。由于食欲素受体的调节在很大程度上尚未确定,我们寻找食欲素受体细胞内尾部的新的蛋白伴侣。我们使用酵母双杂交筛选策略结合共免疫沉淀实验,发现 OX1R 与动力蛋白轻链 Tctex 型 1 和 3(Dynlt1、Dynlt3)之间存在相互作用。这些相互作用被映射到动力蛋白轻链的 C 末端区域和 OX1R 最后 10 个氨基酸内的特定残基上。因此,我们假设动力蛋白轻链可以调节食欲素信号。在表达 OX1R 的 HEK293 细胞中,当共表达 Dynlt1 时,OX-A 刺激产生的细胞外信号调节激酶 1/2(ERK1/2)激活持续时间较短,而在 Dynlt1 表达减少时则延长。位于质膜上的 OX1R 的数量以及 OX-A 诱导的 OX1R 内化(从膜上消失)的动力学和程度均不受 Dynlt1 影响。然而,Dynlt1 减少了 OX1R 在初始内化后在早期内体中的定位。总之,这些数据表明 Dynlt1 通过调节 OX1R 来调节食欲素信号,即在配体诱导内化后调节其细胞内定位。