FIGURE 9.

Schematic model depicting the role for mTOR-mediated phosphorylation of Maf1 in the regulation of Pol III transcription. Shown is a proposed mechanism whereby mTOR regulates Maf1 activity in cancer cells. Top, actively proliferating cells utilize mTOR-mediated phosphorylation of Maf1 to maintain optimal activity of Pol III apparatus. Bottom, inactivation of mTOR by pharmacological inhibitors or due to unfavorable growth conditions leads to enhanced nuclear retention of dephosphorylated Maf1 and repression of new rounds of Pol III synthesis.