Project description:This experiments follows up ChIPseq experiments and aims to investigate the role of Rad50 on gene expression in drosophila larval stage 3 CNS.
Project description:Excessive activation of Hes causes stem cell hyperplasia in larval CNS. Transcriptomics of Notch induced hyperplasia and Hes induced hyperplasia were compared Using affymetrix microarray, global gene expression analysis was performed.
Project description:We assessed the differential expression of genes in the Drosophila larval CNS for the Alk mutant and control to understand how the transcriptional responce in Alk-YS mutant.
Project description:Studies using mice with beta4 nicotinic acetylcholine receptor (nAChR) subunit deficiency (beta4-/- mice) helped reveal the roles of this subunit in bradycardiac response to vagal stimulation, nicotine-induced seizure activity and anxiety. In order to identify genes that might be related to beta4-containing nAChRs activity, we compared the mRNA expression profiles of brains from beta4-/- and wild-type mice using Affymetrix U74Avr2 microarray. Keywords: knockout mice, nicotinic acetylcholine receptor
Project description:Gliogenesis in the Drosophila CNS occurs during embryogenesis and also during the postembryonic larval stages. Several glial subtypes are generated in the postembryonic CNS through the proliferation of differentiated glial cells. The genes and molecular pathways that regulate glial proliferation in the postembryonic CNS are poorly understood. In this study we aimed to use gene expressing profiling of CNS tissue enriched in glia to identify genes expressed in glial cells in the postembryonic CNS. We used microarrays to compare the gene expression profiles from the larval CNS of animals that had increased numbers of glial cells to identify genes that are expressed in glia. RNA was purified from the late third instar larval CNS from control larvae, or larvae expressing an activated form of the FGF receptor (Hlt[ACT]), or overexpressing the insulin receptor (InR) in glial cells using the glial specific driver repoGal4 to increase the number of glial cells and generate CNS tissue enriched in glia.
Project description:Numerous roles for the Alk receptor tyrosine kinase have been described in Drosophila, including functions in the CNS, however the molecular details are poorly understood. To gain mechanistic insight, we employed Targeted DamID (TaDa) transcriptional profiling to identify targets of Alk signaling in the larval CNS. TaDa was employed in larval CNS tissues, while genetically manipulating Alk signaling output. The resulting TaDa data were analysed together with larval CNS scRNA-seq datasets performed under similar conditions, identifying a role for Alk in the transcriptional regulation of neuroendocrine gene expression. Further integration with bulk/scRNA-seq and protein datasets from larval brains in which Alk signaling was manipulated, identified a previously uncharacterized Drosophila neuropeptide precursor encoded by CG4577 as an Alk signaling transcriptional target. CG4577, which we named Sparkly (Spar), is expressed in a subset of Alk-positive neuroendocrine cells in the developing larval CNS, including circadian clock neurons. In agreement with our TaDa analysis, overexpression of the Drosophila Alk ligand Jeb resulted in increased levels of Spar protein in the larval CNS. We show that Spar protein is expressed in circadian (Clock) neurons, and Spar mutants exhibit defects in sleep and circadian rhythm control. In summary, we report a novel activity regulating neuropeptide precursor gene that is regulated by Alk signaling in the Drosophila CNS.