Abstract:
:The mTOR kinase controls cell growth, proliferation, and survival through two distinct multiprotein complexes, mTORC1 and mTORC2. mTOR and mLST8 are in both complexes, while raptor and rictor are part of only mTORC1 and mTORC2, respectively. To investigate mTORC1 and mTORC2 function in vivo, we generated mice deficient for raptor, rictor, or mLST8. Like mice null for mTOR, those lacking raptor die early in development. However, mLST8 null embryos survive until e10.5 and resemble embryos missing rictor. mLST8 is necessary to maintain the rictor-mTOR, but not the raptor-mTOR, interaction, and both mLST8 and rictor are required for the hydrophobic motif phosphorylation of Akt/PKB and PKCalpha, but not S6K1. Furthermore, insulin signaling to FOXO3, but not to TSC2 or GSK3beta, requires mLST8 and rictor. Thus, mTORC1 function is essential in early development, mLST8 is required only for mTORC2 signaling, and mTORC2 is a necessary component of the Akt-FOXO and PKCalpha pathways.
journal_name
Dev Celljournal_title
Developmental cellauthors
Guertin DA,Stevens DM,Thoreen CC,Burds AA,Kalaany NY,Moffat J,Brown M,Fitzgerald KJ,Sabatini DMdoi
10.1016/j.devcel.2006.10.007subject
Has Abstractpub_date
2006-12-01 00:00:00pages
859-71issue
6eissn
1534-5807issn
1878-1551pii
S1534-5807(06)00459-Xjournal_volume
11pub_type
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