PMID:16962829

Citation	Shiota, C, Woo, JT, Lindner, J, Shelton, KD and Magnuson, MA (2006) Multiallelic disruption of the rictor gene in mice reveals that mTOR complex 2 is essential for fetal growth and viability. Dev. Cell 11:583-9
Abstract	The rapamycin-insensitive mTOR complex 2 (mTORC2) has been suggested to play an important role in growth factor-dependent signaling. To explore this possibility further in a mammalian model system, we disrupted the expression of rictor, a specific component of mTORC2, in mice by using a multiallelic gene targeting strategy. Embryos that lack rictor develop normally until E9.5, and then exhibit growth arrest and die by E11.5. Although placental defects occur in null embryos, an epiblast-specific knockout of rictor only delayed lethality by a few days, thereby suggesting other important roles for this complex in the embryo proper. Analyses of rictor null embryos and fibroblasts indicate that mTORC2 is a primary kinase for Ser473 of Akt/PKB. Rictor null fibroblasts exhibit low proliferation rates, impaired Akt/PKB activity, and diminished metabolic activity. Taken together, these findings indicate that both rictor and mTORC2 are essential for the development of both embryonic and extraembryonic tissues.
Links	PubMed Online version:10.1016/j.devcel.2006.08.013
Keywords	Actins/metabolism; Alleles; Animals; Carrier Proteins/metabolism; Cell Proliferation; Cells, Cultured; Embryo, Mammalian/cytology; Fetal Development/genetics; Fetal Viability/genetics; Fibroblasts/metabolism; Fibroblasts/physiology; Gene Targeting; Mice; Mice, Inbred C57BL; Mice, Knockout; Molecular Sequence Data; Protein Kinases/analysis; Protein Kinases/metabolism; Proto-Oncogene Proteins c-akt/metabolism; TOR Serine-Threonine Kinases
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