The InR/Akt/TORC1 Growth-Promoting Signaling Negatively Regulates JAK/STAT Activity and Migratory Cell Fate during Morphogenesis
The InR/Akt/TORC1 Growth-Promoting Signaling Negatively Regulates JAK/STAT Activity and Migratory Cell Fate during Morphogenesis
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InR/Akt/TORC1 生长促进信号在形态发生过程中负向调节 JAK/STAT 活性和迁移细胞命运
DOI：
10.1016/j.devcel.2018.01.017
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发表时间：
2018-02-26
影响因子：
11.8
通讯作者：
Chen, Jiong
中科院分区：
文献类型：
--
作者：
Kang, Di;Wang, Dou;Chen, Jiong
细胞生长和细胞分化是两个不同但又相互关联的发育过程，但它们之间如何协调还不清楚。在果蝇卵子发生过程中，我们发现促进生长的InR/Akt/TOR通路参与抑制迁移边缘细胞的命运决定。InR/Akt/TOR通路通过TOR和Raptor（TORC 1的组分）信号传导，下调JAK/STAT通路，这对于边缘细胞命运决定是必要且充分的。TORC 1通过物理相互作用促进JAK/STAT信号负调控因子SOCS 36 E的蛋白质稳定性，提示TORC 1是协调细胞生长和分化的关键调控因子。
Cell growth and cell differentiation are two distinct yet coupled developmental processes, but how they are coordinatedis not well understood. During Drosophila oogenesis, we found that the growth-promoting InR/Akt/TOR pathway was involved in suppressing the fate determination of the migratory border cells. The InR/Akt/TOR pathway signals through TOR and Raptor, components of TORC1, to downregulate the JAK/STAT pathway, which is necessary and sufficient for border cell fate determination. TORC1 promotes the protein stability ofSOCS36E, theconserved negative regulator of JAK/STAT signaling, through physical interaction, suggesting that TORC1 acts as a key regulator coordinating both cell growth and cell differentiation.