Figure 8.

A model for nutrient/TOR regulation of Pol III in Drosophila. Our data suggest the predominant mechanism by which nutrition/TOR controls Pol III is via Maf1 repression, since Maf1 inhibition completely reverses the decrease in tRNA synthesis caused by TOR inhibition. Myc is sufficient and necessary for Pol III transcription, through controlling levels of Pol III factors (such as Brf) and through interaction with Brf. TOR can control Myc protein levels (Parisi et al, 2011; Teleman et al, 2008—dashed arrow in model figure). But these effects probably do not play a major role in how TOR activates Pol III since our data show that—unlike Maf1 inhibition—maintaining Myc levels and activity cannot reverse the decrease in tRNA synthesis caused by TOR inhibition.