Intrinsic and damage-induced JAK/STAT signaling regulate developmental timing by the Drosophila prothoracic gland.
Intrinsic and damage-induced JAK/STAT signaling regulate developmental timing by the Drosophila prothoracic gland.
复制标题
内在和损伤诱导的 JAK/STAT 信号调节果蝇前胸腺的发育时间
DOI:
10.1242/dmm.049160
复制
发表时间:
2022-01-01
影响因子:
4.3
通讯作者:
Pastor-Pareja JC
中科院分区:
文献类型:
--
作者:
Cao X;Rojas M;Pastor-Pareja JC
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. Summary: Damage signaling from tumors mediated by JAK/STAT-activating Upd cytokines delays the Drosophila larva–pupa transition through co-option of a JAK/STAT developmental role in the prothoracic gland.
登录
查看更多内容
DOI:
10.1016/j.cub.2010.01.038
发表时间:
2010-03-09
期刊:
Current biology : CB
影响因子:
--
作者:
Halme A;Cheng M;Hariharan IK
通讯作者:
Hariharan IK
影响因子:
4.5
作者:
Akai N;Ohsawa S;Sando Y;Igaki T
通讯作者:
Igaki T
影响因子:
1.2
作者:
Bach, Erika A.;Ekas, Laura A.;Baeg, Gyeong-Hun
通讯作者:
Baeg, Gyeong-Hun
影响因子:
11.4
作者:
Eulenberg, KG;Schuh, R
通讯作者:
Schuh, R
影响因子:
9.2
作者:
Boulan, Laura;Martin, David;Milan, Marco
通讯作者:
Milan, Marco