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

被引:10
|
作者
Kang, Di [1 ,2 ]
Wang, Dou [1 ,2 ]
Xu, Jianbing [1 ,2 ]
Quan, Chao [1 ,2 ]
Guo, Xuan [1 ,2 ]
Wang, Heng [1 ,2 ]
Luo, Jun [1 ,2 ]
Yang, Zhongzhou [1 ,2 ]
Chen, Shuai [1 ,2 ]
Chen, Jiong [1 ,2 ]
机构
[1] Nanjing Univ, Model Anim Res Ctr, State Key Lab Pharmaceut Biotechnol, 12 Xue Fu Rd, Nanjing 210061, Jiangsu, Peoples R China
[2] Nanjing Univ, Model Anim Res Ctr, MOE Key Lab Model Anim Dis Study, 12 Xue Fu Rd, Nanjing 210061, Jiangsu, Peoples R China
关键词
DROSOPHILA-OOGENESIS; FEEDBACK INHIBITION; STEM-CELLS; PATHWAY; RAPAMYCIN; SIZE; PROTEIN; MTOR; PROLIFERATION; GRADIENT;
D O I
10.1016/j.devcel.2018.01.017
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:524 / +
页数:13
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