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Response to Comment on “A Dynamic Network Model of mTOR Signaling Reveals TSC-Independent mTORC2 Regulation”: Building a Model of the mTOR Signaling Network with a Potentially Faulty Tool

Dalle Pezze et al. respond to criticisms regarding the specificity of phosphorylation of Ser2481 of mTOR as a specific readout of mTORC2 activity. We modeled the mammalian or mechanistic target of rapamycin (mTOR) network and proposed a previously unknown mode of activation of the mTOR-containing complex mTORC2 through a phosphoinositide 3-kinase–dependent, and tuberous sclerosis complex–independent mechanism. Manning questions the validity of using the phosphorylation of Ser2481 of mTOR as a specific readout of mTORC2 activity and suggests an in vitro mTORC2 kinase assay as a more appropriate method to parameterize a dynamic mTOR model. We maintain that our computational-experimental approach in combination with careful selection of the readout and cell system is appropriate for studying mTORC2 regulation by insulin.