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editorial
. 2014 Mar 15;1(2):111–112. doi: 10.18632/oncoscience.15

Figure 1. A model of nutrient-dependent regulation of NML-SirT1 interaction.

Figure 1

(a) During nutrient-rich growth, mTOR stimulates RNA Pol I and Pol III synthesis of rRNA. The nascent rRNA in turn binds to NML and inhibits eNoSC assembly on rDNA, providing a positive feedback to amplify mTOR signaling. (b) During starvation, mTOR inactivation reduces Pol I and Pol III activity. Reduced nascent rRNA level enables NML to bind and recruit SirT1 to the nucleolus, promoting heterochromatin formation and silencing of the rDNA.