論文 - 詳細
| RRC ID | 69049 |
|---|---|
| 著者 | Cao X, Rojas M, Pastor-Pareja JC. |
| タイトル | Intrinsic and damage-induced JAK/STAT signaling regulate developmental timing by the Drosophila prothoracic gland. |
| ジャーナル | Dis Model Mech |
| Abstract |
Development involves tightly paced, reproducible sequences of events, yet it must adjust to conditions external to it, such as resource availability and organismal damage. A major mediator of damage-induced immune responses in vertebrates and insects is JAK/STAT signaling. At the same time, JAK/STAT activation by the Drosophila Upd cytokines is pleiotropically involved in normal development of multiple organs. Whether inflammatory and developmental roles of JAK/STAT intersect is unknown. Here, we show that JAK/STAT is active during development of the prothoracic gland (PG), the organ that controls metamorphosis onset through ecdysone production. Reducing JAK/STAT signaling decreased PG size and slightly advanced metamorphosis. Conversely, JAK/STAT hyperactivation, achieved through overexpression of pathway components or SUMOylation loss, caused PG hypertrophy and metamorphosis delay. Interestingly, tissue damage and tumors, known to secrete Upd cytokines, also activated JAK/STAT in the PG and delayed metamorphosis. Finally, we show that expression of transcription factor Apontic, a JAK/STAT target in the PG, recapitulates PG hypertrophy and metamorphosis delay. JAK/STAT damage signaling, therefore, regulates metamorphosis onset at least in part by coopting its developmental role in the PG. |
| 巻・号 | 15(1) |
| 公開日 | 2022-1-1 |
| DOI | 10.1242/dmm.049160 |
| PII | 273570 |
| PMID | 34842272 |
| PMC | PMC8807578 |
| MeSH | Animals Drosophila* Drosophila Proteins* / metabolism Drosophila melanogaster / metabolism Ecdysone / metabolism Gene Expression Regulation, Developmental Signal Transduction / physiology |
| IF | 4.651 |
| オルトメトリクス指標 |
オルトメトリクス指標項目
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| 最多言及媒体 | X(Twitter) |
| 各媒体での言及数の合計 | 7 |
| 過去6か月間でのオルトメトリクス指標の変動値 | 0.0 |
| リソース情報 | |
| ショウジョウバエ | 4257R-2 5993R-2 8068R-2 8068R-1 |