RNA-seq of regenerating blastema cells in Drosophila melanogaster
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ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE101797 | GEO | 2017/07/25
SECONDARY ACCESSION(S): PRJNA395544
REPOSITORIES: GEO
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Project description:An important unanswered question in regenerative biology is to what extent regeneration is accomplished by the reactivation of gene regulatory networks used during development versus the activation of regeneration-specific transcriptional programs. Following damage, Drosophila imaginal discs, the larval precursors of adult structures, can regenerate missing portions by localized proliferation of damage-adjacent tissue. Using single-cell transcriptomics in regenerating wing discs, we have obtained a comprehensive view of the transcriptome of regenerating discs and identified two regeneration-specific cell populations within the blastema, Blastema1 and Blastema2. Collectively, these cells upregulate multiple genes encoding secreted proteins that promote regeneration including Pvf1, upd3, asperous, Mmp1, and the maturation delaying factor Ilp8. Expression of the transcription factor Ets21C is restricted to this regenerative secretory zone; it is not expressed in undamaged discs. Ets21C expression is activated by the JNK/AP-1 pathway, and it can function in a type 1 coherent feedforward loop with AP-1 to sustain expression of downstream genes. Without Ets21C function, the blastema cells fail to maintain the expression of a number of genes, which leads to premature differentiation and severely compromised regeneration. As Ets21C is dispensable for normal development, these observations indicate that Ets21C orchestrates a regeneration-specific gene regulatory network. We have also identified cells resembling both Blastema1 and Blastema2 in scribble tumorous discs. They express the Ets21C-dependent gene regulatory network, and eliminating Ets21C function reduces tumorous growth. Thus, mechanisms that function during regeneration can be co-opted by tumors to promote aberrant growth.
2022-07-10 | GSE174326 | GEO
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.
2017-09-30 | GSE94938 | GEO
Project description:Chromatin landscape changes of regenerating wing imaginal discs
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Project description:Regeneration of fragmented Drosophila imaginal discs occurs in an epimorphic manner, involving local cell proliferation at the wound site. Following disc fragmentation, cells at the wound site activate a restoration program through wound healing, regenerative cell proliferation and repatterning of the tissue. However, the interplay of signaling cascades, driving these early reprogramming steps, is not well understood. Here we profiled the transcriptome of regenerating cells in the early phase within twenty-four hours after wounding. We found that JAK/STAT signaling becomes activated at the wound site and promotes regenerative cell proliferation in cooperation with Wingless (Wg) signaling. In addition, we demonstrated that the expression of Drosophila insulin-like peptide 8 (dilp8), which encodes a paracrine peptide to delay the onset of pupariation, is controlled by JAK/STAT signaling in early regenerating discs. Our findings suggest that JAK/STAT signaling plays a pivotal role in coordinating regenerative disc growth with organismal developmental timing. In order to analyze transcriptome change in early regenerating imaginal disc, Drosophila prothorasic leg discs were fragmented (to anterior one-quarter or posterior three-quarters) and cultured ex vivo in adult fly abdomen. Regenerating cells in early regeneration phase (at 12 or 24 hours after wounding) were subjected to transcriptome profiling with Affymetrix microarrays. For control samples, the corresponding regions of uncut-cultured discs and uncut-uncultured discs were used.
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Project description:Microarray comparison of anterior and posterior Drosophila wing imaginal disc cells
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Project description:Mechanisms of tumor-cells-invasion in Drosophila wing imaginal disc epithelia
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Project description:Hox proteins have been proposed to act at multiple levels within regulatory hierarchies and to directly control the expression of a plethora of target genes. However, for any specific Hox protein or tissue, very few direct in vivo-regulated target genes have been identified. Here, we have identified target genes of the Hox protein Ultrabithorax (UBX), which modifies the genetic regulatory network of the wing to generate the haltere, a modified hindwing. We used whole-genome microarrays and custom arrays including all predicted transcription factors and signaling molecules in the D. melanogaster genome to identify differentially expressed genes in wing and haltere imaginal discs. To elucidate the regulation of selected genes in more detail, we isolated cis-regulatory elements (CREs) for genes that were specifically expressed in either the wing disc or haltere disc. We demonstrate that UBX binds directly to sites in one element, and these sites are critical for activation in the haltere disc. These results indicate that haltere and metathoracic segment morphology is not achieved merely by turning off the wing and mesothoracic development programs, but rather specific genes must also be activated to form these structures. The evolution of haltere morphology involved changes in UBX-regulated target genes, both positive and negative, throughout the wing genetic regulatory network. Keywords: tissue comparison
2006-11-23 | GSE6307 | GEO
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.
2021-09-09 | PXD019761 | Pride