The Tsc1-Tsc2 complex influences neuronal polarity by modulating TORC1 activity and SAD levels.

Neuronal function depends on the specification of neuronal processes as axons or dendrites. In this issue of Genes & Development Choi and colleagues (2485-2495) show that without Tuberous Sclerosis Complex 1 (Tsc1) or Tsc2, molecules linked to the autosomal dominant disease tuberous sclerosis, an increase in the activity of the translational regulator Target of Rapamycin 1 (TORC1) causes neurons to have multiple axons and the translation of SAD kinase increases as well. Thus, in addition to the kinase LKB1, the Tsc1-Tsc2 complex, acting through TORC1, also modulates SAD to regulate axon formation.