The InR/Akt/TORC1 Growth-Promoting Signaling Negatively Regulates JAK/STAT Activity and Migratory Cell Fate during Morphogenesis

Publication date: Available online 15 February 2018
Source:Developmental Cell
Author(s): Di Kang, Dou Wang, Jianbing Xu, Chao Quan, Xuan Guo, Heng Wang, Jun Luo, Zhongzhou Yang, Shuai Chen, Jiong Chen
Cell growth and cell differentiation are two distinct yet coupled developmental processes, but how they are coordinated is 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 of SOCS36E, the conserved negative regulator of JAK/STAT signaling, through physical interaction, suggesting that TORC1 acts as a key regulator coordinating both cell growth and cell differentiation.

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Teaser

Kang, Wang et al. examine cell growth and cell differentiation coupling in the context of migratory border cell fate specification in Drosophila. They show that the growth-promoting InR/Akt/TORC1 pathway controls the protein stability of the JAK/STAT pathway negative regulator SOCS36E, via direct binding by TORC1, to control fate determination.


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