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

• DOI: 10.1016/j.devcel.2018.01.017
• Publication Date: 2018-02-15T16:38:35Z
• Authors: Di Kang; Dou Wang; Jianbing Xu; Chao Quan; Xuan Guo; Heng Wang; Jun Luo; Zhongzhou Yang; Shuai Chen; Jiong Chen
• Keywords: 0301 basic medicine; Gene Expression Regulation, Developmental; Receptor Protein-Tyrosine Kinases; Cell Differentiation; Janus Kinase 1; STAT Transcription Factors; 03 medical and health sciences; Drosophila melanogaster; Cell Movement; Proteolysis; Morphogenesis; Animals; Drosophila Proteins; Phosphorylation; Proto-Oncogene Proteins c-akt; Signal Transduction; Transcription Factors

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.