The mechanistic target of rapamycin (mTOR) controls various cellular processes and forms two distinct complexes, mTORC1 and mTORC2. mTORC1 includes the Raptor subunit and mTORC2 includes the Rictor subunit. It has been recently reported that mTOR regulates cellular functions through complexes-independent role in a context-dependent manner, in addition to through complexes-dependent role. In this study, we generated and analyzed conditional mutant embryos to establish the pivotal role of mTOR in skeletal development. Conditional deletion of either Mtor, Raptor, or Rictor genes in undifferentiated mesenchymal cells or chondrocytes led to skeletal dysfunctions. Simultaneous deletion of Raptor and Rictor in undifferentiated mesenchymal cells resembled the skeletal phenotypes of Mtor deficient embryos. In contrast, simultaneous deficiency of Raptor and Rictor in chondrocytes displayed milder skeletal defects when compared with Mtor deficiency. These findings indicate that mTOR regulates skeletal development mainly through complex-dependent in undifferentiated mesenchymal cells, whereas mTOR regulates skeletal development at least in part through complex-independent pathway in chondrocytes.