期刊
GENES & DEVELOPMENT
卷 27, 期 24, 页码 2642-2647出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.225169.113
关键词
Notch; PINK1; mTORC2/AKT signaling; mitochondria; neural stem cells; cancer stem cells
资金
- National Institutions of Health [R01 NS043167, R01 AR054926]
- Stanford University School of Medicine Dean's Post-doctoral Fellowship
The self-renewal versus differentiation choice of Drosophila and mammalian neural stem cells (NSCs) requires Notch (N) signaling. How N regulates NSC behavior is not well understood. Here we show that canonical N signaling cooperates with a noncanonical N signaling pathway to mediate N-directed NSC regulation. In the noncanonical pathway, N interacts with PTEN-induced kinase 1 (PINK1) to influence mitochondrial function, activating mechanistic target of rapamycin complex 2 (mTORC2)/AKT signaling. Importantly, attenuating noncanonical N signaling preferentially impaired the maintenance of Drosophila and human cancer stem cell-like tumor-forming cells. Our results emphasize the importance of mitochondria to N and NSC biology, with important implications for diseases associated with aberrant N signaling.
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