MiR-969 And Sin3A Regulate Drosophila Motorneuron Function And Notch Signaling Pathway Respectively

The first part of my thesis mainly discussed the expression pattern and molecular function of miR-969 in Drosophila motor neurons.We found that miR-969 was highly expressed in motor neurons during Drosophila development,from embryonic stage to adult stage.When miR-969 was knocked out,mutant showed climbing disability.Furthermore,Drosophila showed similar climbing disability when miR-969 was specifically knocked down in Drosophila motor neurons by miR-969 sponge with D42-gal4,OK371-gal4 and miR-969 gal4.We used bioinformatics methods to find two potential target genes Pak3 and kay,which were reported to affect the function of Drosophila motor neurons.When either Pak3 or kay was knocked down in miR-969 mutant,it could appropriately rescue the climbing phenotype.In addition,we used Dual-Luciferase Reporter Assay in Drosophila S2 cell to verify that miR-969 could directly regulate kay 3'UTR.In conclusion,miR-969 negatively regulates target gene kay to participate in controlling the function of Drosophila motor neurons.The second part of my thesis mainly discussed the participation of Sin3A in regulating Notch signaling pathway.We firstly found that the expression of Notch target genes cut,wg,E(spl)m8 and Su(H)were decreased when Sin3A was knocked down in Drosophila wingdisc.And koncking down of Sin3A caused wing Notching.Overexpression of Notch but not Delta could resuce the reduction of Notch target genes caused by knocking down Sin3A.What is more,knockdown of Sin3A caused downregulation of Notch transcription levels.In summary,these results suggest that Sin3A acts upstream of Notch and regulates the transcription levels of Notch.