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• W3216839904 abstract "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 JAK/STAT roles intersect is unknown. Here, we show that JAK/STAT is active during development of the prothoracic gland (PG), which controls metamorphosis onset through ecdysone production. Reducing JAK/STAT signaling decreased PG size and advanced metamorphosis. Conversely, JAK/STAT hyperactivation by overexpression of pathway components or SUMOylation loss caused PG hypertrophy and metamorphosis delay. Tissue damage and tumors, known to secrete Upd cytokines, also activated JAK/STAT in the PG and delayed metamorphosis, at least in part by inducing expression of the JAK/STAT target Apontic. JAK/STAT damage signaling, therefore, regulates metamorphosis onset by co-opting its developmental role in the PG. Our findings in Drosophila provide insights on how systemic effects of damage and cancer can interfere with hormonally controlled development and developmental transitions." @default.
• W3216839904 created "2021-12-06" @default.
• W3216839904 creator A5017035217 @default.
• W3216839904 creator A5065574971 @default.
• W3216839904 creator A5076525253 @default.
• W3216839904 date "2022-01-01" @default.
• W3216839904 modified "2023-10-05" @default.
• W3216839904 title "Intrinsic and damage-induced JAK/STAT signaling regulate developmental timing by the <i>Drosophila</i> prothoracic gland" @default.
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• W3216839904 doi "https://doi.org/10.1242/dmm.049160" @default.
• W3216839904 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34842272" @default.
• W3216839904 hasPublicationYear "2022" @default.
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