Project description:Comparative analysis of gene expression changes upon overexpression of activated Thickveins in the Drosophila wing at larval vs. pupal stages
Project description:Screening for binding partners of the splicing factor SmD3 and changes in interaction upon depletion of the protein Ecdysoneless (Ecd) in the nubbin domain of third-instar larval wing imaginal discs.
Project description:The systemic response to injury in Drosophila melanogaster is characterized by the activation of specific signaling pathways that facilitate the regeneration of wounded tissue and help coordinate wound healing with organism growth. The mechanisms by which damaged tissues influence the development and function of peripheral non-injured tissues is not fully understood. Injury was induced in early third instar larvae via temperature-dependent cell death in wing imaginal discs. Microarray analysis using RNA isolated from injured and control was used to identify genes underlying the systemic injury response. We identified 150 genes which were differentially expressed in response to localized cell death in wing imaginal discs. Upregulated genes were associated biological processes including carnitine biosynthesis, signal transduction and regulation of oxidoreductase activity while terms associated with downregulated genes included wound healing, imaginal disc-derived wing hair outgrowth, and regulation of glutamatergic synaptic transmission. Pathway analysis revealed that wing disc damage led to changes in fatty acid, cysteine, and carnitine metabolism. One gene, 14-3-3ζ, which encodes a known regulator of Ras/MAPK signaling was identified as a potential regulator of transdetermination during tissue regeneration. Our results raise the possibility that immune function and cell proliferation during wing disc repair and regeneration in Drosophila may require the sulfur amino acid cysteine and its’ metabolites, taurine and glutathione, similar to what has been reported during tissue repair in mammals. Further, it seems likely that imaginal disc damage stimulates the mobilization of fatty acids to support the energetically demanding process of tissue regeneration. The roles of additional genes that are differentially regulated following imaginal disc injury remain to be elucidated.
