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Cell migration

MTORC2 brings up the rear

Nature Reviews Molecular Cell Biology volume 12, pages 74–75 (2011)Cite this article

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To assess the importance of mTORC2 in neutrophil chemotaxis, the authors used short hairpin RNA to suppress the mTORC2 component rapamycin-insensitive companion of mTOR (RICTOR). This led to marked defects in neutrophil migration towards the chemoattractant fMLP as well as in polarization, although actin polymerization was comparable to control cells. The effects of RICTOR were mediated by its downstream target protein kinase C (PKC), as inhibition of PKC abrogated neutrophil chemotaxis to fMLP and led to defective retraction of the cell rear.

In D. discoideum, TORC2 regulates the activity of adenylyl cyclase A (ACA), which synthesizes cyclic AMP in response to chemotactic stimulation. cAMP can then regulate chemotaxis by inhibiting pseudopod formation or can be secreted and act as a chemoattractant. The authors found that mTORC2 also regulates cAMP synthesis in neutrophils, through PKC-mediated activation of the AC9 isoform. Specifically, although control cells showed increased cAMP levels in response to fMLP, this was not observed with RICTOR- or PKC-deficient neutrophils. Furthermore, AC9-deficient neutrophils had lower intracellular cAMP levels than controls, showed no increase in cAMP levels in response to fMLP and had defects in chemotaxis, indicating an essential role for cAMP in this process.

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ORIGINAL RESEARCH PAPER

  1. Liu, L. et al. mTORC2 regulates neutrophil chemotaxis in a cAMP- and RhoA-dependent fashion. Dev. Cell 19, 845–857 (2010) Article

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  1. Rachel David
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David, R. MTORC2 brings up the rear. Nat Rev Mol Cell Biol 12, 74–75 (2011). https://doi.org/10.1038/nrm3046

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