Abstract
Sexually dimorphic phenotypes are a universal phenomenon in animals. In the model animal fruit fly Drosophila, males and females exhibit long- and short-sleep phenotypes, respectively. However, the mechanism is still a mystery. In this study, we showed that juvenile hormone (JH) is involved in regulation of sexually dimorphic sleep in Drosophila, in which gain of JH function enlarges differences of the dimorphic sleep phenotype with higher sleep in males and lower sleep in females, while loss of JH function blurs these differences and results in feminization of male sleep and masculinization of female sleep. Further studies indicate that germ cell-expressed (GCE), one of the JH receptors, mediates the response in the JH pathway because the sexually dimorphic sleep phenotypes cannot be rescued by JH hormone in a gce deletion mutant. The JH-GCE regulated sleep dimorphism is generated through the sex differentiation-related genes -fruitless (fru) and doublesex (dsx) in males and sex-lethal (sxl), transformer (tra) and doublesex (dsx) in females. These are the “switch” genes that separately control the sleep pattern in males and females. Moreover, analysis of sleep deprivation and circadian behaviors showed that the sexually dimorphic sleep induced by JH signals is a change of sleep drive and independent of the circadian clock. Furthermore, we found that JH seems to also play an unanticipated role in antagonism of an aging-induced sleep decrease in male flies. Taken together, these results indicate that the JH signal pathway is critical for maintenance of sexually dimorphic sleep by regulating sex-relevant genes.
Highlights
Sleep is a general phenomenon identified in many species and is usually accompanied with various sex-specific properties
We reported that Juvenile hormone (JH) induces completely different sleep effects between males and females with higher sleep in males and lower sleep in females, while loss of Juvenile Hormone (JH) function blurs these differences and results in feminization of male sleep and masculinization of female sleep
Further studies indicate that the sexual dimorphism of sleep is generated through the sex differentiation-related genes regulated by JH and its receptor germ cell-expressed (GCE) signaling
Summary
Sleep is a general phenomenon identified in many species and is usually accompanied with various sex-specific properties. There are sex differences in responses of male and female rats to sleep deprivation[2]. Previous studies reported that there is a large sex difference in the total sleep amounts during the daylight hours, in which female sleep is only 40% of male sleep in D. melanogaster [6].To address that phenomenon, specific neurons[7,8] and non-neural factors [8] relevant to sexually dimorphic sleep have been discussed. Other types of sexual dimorphism (e.g., stress resistance, feeding, and physical characteristics) mediated by insulin, dopamine and Juvenile Hormone (JH) may participate in the relevant regulatory circuits[9,10], but their specific interactions and the molecular mechanism are still unclear. We examine the role of JH in the control of a sexually dimorphic sleep phenotype
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