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A more recent version of this article appeared on March 1, 2007
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Submitted on May 9, 2006
Revised on December 20, 2006
Accepted on December 29, 2006
Department of Pharmacology and Cancer Institute of New Jersey (CINJ), Robert Wood Johnson Medical School, Piscataway, NJ 08854
Monitoring Editor: Carole Parent
Mammalian target of rapamycin (mTOR) forms two complexes, mTORC1 and mTORC2 that play central roles in cell growth and functions. Only mTORC1 is directly inhibited by the immunosuppressive drug rapamycin. Despite recent progress in identifying new components and functions of the mTOR pathway, relatively little is known about the spatial arrangement of mTOR signaling and the underlying mechanisms. In a previous study, we showed that a large proportion of mTOR is localized to the ER and Golgi in many common cell lines. Here we report the identification of an internal mTOR sequence that contains two HEAT (HT) repeats, HT18/19, and two intervening interunit spacers (IUS) 17/18, which is sufficient to target EGFP to the Golgi. Surprisingly, deletion of IUS17 from this Golgi localization sequence (GLS) converts it to an ER localization sequence (ELS). Deletion of HT19, a common element of both GLS and ELS from the full length mTOR, causes delocalization of mTOR, and inhibits the ability of mTOR to promote S6 phosphorylation. Moreover, overexpression of GLS and ELS inhibits both mTOR complexes. Together, our results reveal unusual ER- and Golgi-targeting sequences, and suggest that anchoring to these organelles is important for the functions of mTOR complexes.
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