Local ecdysone synthesis in a wounded epithelium sustains developmental delay and promotes regeneration in Drosophila.
Local ecdysone synthesis in a wounded epithelium sustains developmental delay and promotes regeneration in Drosophila.
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受伤上皮中的局部蜕皮激素合成维持果蝇的发育延迟并促进再生。
DOI：
10.1101/2024.02.25.581888
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发表时间：
2024
期刊：
影响因子：
--
通讯作者：
Moberg,Kenneth
中科院分区：
文献类型：
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作者：
Terry,Douglas;Schweibenz,Colby;Moberg,Kenneth
再生能力通常随着动物成熟超过胚胎和幼年阶段而下降，这表明再生需要重新定向促进发育生长的生长途径。有趣的是，果蝇幼虫的上皮细胞需要激素蜕皮激素（Ec）来生长，但需要循环中Ec水平的下降来再生。检查EC动力学更密切，我们发现，EC受体（EcR）的转录活性下降，在未受伤的地区的翼盘，但同时上升周围的细胞损伤诱导的芽基。与此同时，芽基耗尽编码Ec生物合成酶的基因阻断了EcR的活性，损害了再生，但对未受伤的翅膀没有影响。我们发现，局部Ec/EcR信号是损伤诱导的损伤后的蜕皮延迟所必需的，并且关键的再生调节因子supd 3和Ets 21 c对Ec水平作出反应。总的来说，这些数据表明，损伤诱导的本地来源的EC内的翼芽，维持必要的发育迟缓和组织修复的转录签名。
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, theDrosophilalarval 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 regulatorsupd3andEts21crespond 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.