Regulation Of Sleep By Insulin-like Peptide And Its Receptor In Drosophila Melanogaster

Sleep behavior is widespread from insects to mammals, and is very important for maintaining normal life. Drosophila melanogaster as a model organism for study of sleep provides reference for human. Insulin is one of the most widely studied peptide hormones, and the insulin/IGF signaling (ⅡS) pathway plays a key role in growth, development, metabolism, longevity, reproduction and stress resistance in diverse organisms including mammals. According to the report that NPF locating in the downstream of DILP regulates sleep, we investigated the functions of DILPS and its receptor DInR on sleep in Drosophila melanogaster. The main results are as follows:1Under the condition of LD and DD, DILPs and DInR regulate sleep behaviour in Drosophila melanogaster. dilpl-7and dinr deficient mutant strains (except for dilpA) significantly decrease the total sleep time during ZTO-12, and dilp3also reduces the total sleep time during ZT12-24. Up regulation of dilp2and dinr obviously increase the total sleep time during ZTO-12and ZT12-24, principally caused by reduction of sleep bout duration.2Under the condition of LD and DD, up regulation of DILPs in clock neurons affect sleep in Drosophila melanogaster. Up-regulated expression of dilp2in cry-expression clock neurons increase the total sleep during ZTO-12and ZT12-24, and the rising rate of daytime-sleep is more obvious. Up-regulated of dilp2in pdf-expression clock neurons increase the total sleep during ZTO-12, and there is no difference between controls and treatment during ZT12-24.3DILPs and DInR have no effects on endogenous circadian rhythm in Drosophila melanogaster. Neither dilpl-7or dinr deficient mutant strains nor over-expression of dilp2or dinr has influence on endogenous locomotor rhythm, nor does over-expression of dilp2in clock neurons. The results illustrate endogenous circadian rhythm does not affect the regulation of DILPs and DInR on sleep.