<P><B>Summary</B></P> <P>Target of rapamycin complex 1 (TORC1) regulates cell growth in response to nutrients and growth factors. Although TORC1 signaling has been thoroughly studied at the cellular level, the regulation...
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https://www.riss.kr/link?id=A107429426
2017
-
Drosophila TORC1 ; Hedgehog ; E2F1 ; cell cycle ; S6K
SCI,SCIE,SCOPUS
학술저널
363-3754(3392쪽)
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
<P><B>Summary</B></P> <P>Target of rapamycin complex 1 (TORC1) regulates cell growth in response to nutrients and growth factors. Although TORC1 signaling has been thoroughly studied at the cellular level, the regulation...
<P><B>Summary</B></P> <P>Target of rapamycin complex 1 (TORC1) regulates cell growth in response to nutrients and growth factors. Although TORC1 signaling has been thoroughly studied at the cellular level, the regulation of TORC1 in multicellular tissues and organs has remained elusive. Here we found that TORC1 is selectively activated in the second mitotic wave (SMW), the terminal synchronous cell division, of the developing <I>Drosophila</I> eye. We demonstrated that Hedgehog (Hh) signaling regulates TORC1 through E2F1 and the cyclin D/Cdk4 complex in the SMW, and this regulation is independent from insulin and amino acid signaling pathways. TORC1 is necessary for the proper G1/S transition of the cells, and the activation of TORC1 rescues the cell-cycle defect of Hh signaling-deficient cells in the SMW. Based on this evolutionarily conserved regulation of TORC1 by Hh signaling, we propose that Hh-dependent developmental signaling pathways spatially regulate TORC1 activity in multicellular organisms.</P> <P><B>Highlights</B></P> <P> <UL> <LI> TORC1 is selectively active in the second mitotic wave (SMW) of <I>Drosophila</I> eye disc </LI> <LI> Hedgehog activates TORC1 independently of insulin and amino acid signaling </LI> <LI> TORC1 regulates G1/S transition downstream of Hh signaling in the SMW </LI> <LI> TORC1 regulation by Hedgehog is conserved in mammalian cells </LI> </UL> </P> <P><B>Graphical Abstract</B></P> <P>[DISPLAY OMISSION]</P>