RESUMO
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.
Assuntos
Drosophila melanogaster/genética , Hormônios Juvenis/metabolismo , Transdução de Sinais , Sono/genética , Animais , Proteínas de Ligação a DNA/genética , Proteínas de Ligação a DNA/metabolismo , Proteínas de Drosophila/genética , Proteínas de Drosophila/metabolismo , Drosophila melanogaster/metabolismo , Feminino , Expressão Gênica , Masculino , Mutação , Proteínas do Tecido Nervoso/genética , Proteínas do Tecido Nervoso/metabolismo , Fenótipo , Proteínas de Ligação a RNA/genética , Proteínas de Ligação a RNA/metabolismo , Fatores Sexuais , Fatores de Tempo , Fatores de Transcrição/genética , Fatores de Transcrição/metabolismoRESUMO
The corn borer is a world-wide agricultural pest. In this study, a full-length neuropeptide F (npf) gene in Ostrinia furnacalis was sequenced and cloned from a cDNA library, in which the npf gene produces two splicing mRNA variants - npf1 and npf2 (with a 120 bp segment inserted into the npf1 sequence to generate npf2). A spatio-temporal expression analysis showed that the highest expression level of npf was in the midgut of 5th instar larvae (the gluttony period), and their npf expression and food consumption were significantly promoted after food deprivation for 6 h. When npf was knocked down by double-stranded RNA for NPF, larval food intake, weight and body size were effectively inhibited through changes of a biosynthesis and metabolism pathway; i.e. gene silencing of NPF causes decreases of total lipid and glycogen and increases of trehalose production. Moreover, we produced transgenic corn plants with stably expressed dsNPF. Results showed that O. furnacalis larvae fed on these transgenic leaves had lower food consumption and smaller body size compared to controls. These results indicate that NPF is important in the feeding control of O. furnacalis and valuable for production of potential transgenic corn.
