The Tsc1–Tsc2 complex influences neuronal polarity by modulating TORC1 activity and SAD levels: Figure 1.

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Abstract
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.