Pten is involved in the suppressing the Akt signaling pathway upstream of mTOR activity, which normally leads to dephosphorylation of FMRP and subsequent protein translation. However, there is some evidence that suggests Pten might be acting differently. In particular, deletion of Pten leads to decreased expression of mGluR5, increased expression of FMRP, and increased phosphorylation of FMRP (Lugo et al., 2014). These findings seem to oppose, rather than overlap with, findings from Fmr1 knockout mice. More work needs to be done to determine the molecular consequences of Pten loss-of-function and how this contributes to ASD-like phenotypes.
