Abstract
Sleep is an important, well-conserved behavior throughout all the species. When an\r animal is sleep deprived, it increases the amount of sleep the following day to make up for the\r lost sleep, called “rebound sleep.” We have identified many microRNAs that regulate sleep and\r microRNA-190 is one of them. MicroRNAs are small, non-coding RNAs that are 21-25\r nucleotides long, which bind to mRNAs and prevent their translation. Previous studies in the\r Griffith lab have identified mircoRNA-190 as a regulator of sleep. MicroRNA190 inhibition\r causes decreased and fragmented nighttime sleep. Our research seeks to determine whether\r miR190 affects sleep homeostasis by regulating neurons. We inhibited miR190 function using\r Gal4/UAS system that can be used for cell-type specific expression to control the expression of\r the miR inhibitor called a “miR sponge.” MicroRNA sponge soaks up the microRNA and\r prevents it from binding to their mRNA targets. We initially expressed miR sponge in the\r neurons using neurons specific Gal4 driver called, NsybGal4 and cholinergic neuron specific\r driver called, ChaGal4 and observed the changes in baseline sleep and sleep homeostasis of these\r flies. Sleep homeostasis is the ability to detect low levels of sleep and subsequently produce a\r compensatory increase in sleep (called “rebound sleep”). We found that flies with inhibited\r miR190 function in both neurons and cholinergic neurons had less nighttime sleep and increased\r rebound sleep. Flies recovered most of their sleep during nighttime.