{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Terry D"],"funding":["NCI NIH HHS","NIGMS NIH HHS"],"pubmed_abstract":["Regenerative ability often declines as animals mature past embryonic and juvenile stages, suggesting that regeneration requires redirection of growth pathways that promote developmental growth. Intriguingly, the <i>Drosophila</i> larval epithelia require the hormone ecdysone (Ec) for growth but require a drop in circulating Ec levels to regenerate. Examining Ec dynamics more closely, we find that transcriptional activity of the Ec-receptor (EcR) drops in uninjured regions of wing discs, but simultaneously rises in cells around the injury-induced blastema. In parallel, blastema depletion of genes encoding Ec biosynthesis enzymes blocks EcR activity and impairs regeneration but has no effect on uninjured wings. We find that local Ec/EcR signaling is required for injury-induced pupariation delay following injury and that key regeneration regulators <i>upd3</i> and <i>Ets21c</i> respond to Ec levels. Collectively, these data indicate that injury induces a local source of Ec within the wing blastema that sustains a transcriptional signature necessary for developmental delay and tissue repair."],"journal":["bioRxiv : the preprint server for biology"],"pagination":["2024.02.25.581888"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10925115"],"repository":["biostudies-literature"],"pubmed_title":["Local ecdysone synthesis in a wounded epithelium sustains developmental delay and promotes regeneration in <i>Drosophila</i>."],"pmcid":["PMC10925115"],"funding_grant_id":["R01 GM121967","F31 CA239563","R01 GM123136"],"pubmed_authors":["Schweibenz C","Moberg K","Terry D"],"additional_accession":[]},"is_claimable":false,"name":"Local ecdysone synthesis in a wounded epithelium sustains developmental delay and promotes regeneration in <i>Drosophila</i>.","description":"Regenerative ability often declines as animals mature past embryonic and juvenile stages, suggesting that regeneration requires redirection of growth pathways that promote developmental growth. Intriguingly, the <i>Drosophila</i> larval epithelia require the hormone ecdysone (Ec) for growth but require a drop in circulating Ec levels to regenerate. Examining Ec dynamics more closely, we find that transcriptional activity of the Ec-receptor (EcR) drops in uninjured regions of wing discs, but simultaneously rises in cells around the injury-induced blastema. In parallel, blastema depletion of genes encoding Ec biosynthesis enzymes blocks EcR activity and impairs regeneration but has no effect on uninjured wings. We find that local Ec/EcR signaling is required for injury-induced pupariation delay following injury and that key regeneration regulators <i>upd3</i> and <i>Ets21c</i> respond to Ec levels. Collectively, these data indicate that injury induces a local source of Ec within the wing blastema that sustains a transcriptional signature necessary for developmental delay and tissue repair.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Feb","modification":"2026-06-27T03:17:10.792Z","creation":"2025-04-06T17:25:43.949Z"},"accession":"S-EPMC10925115","cross_references":{"pubmed":["38464192"],"doi":["10.1101/2024.02.25.581888"]}}