Figure 7: Model of Mep2 regulation by the TORC1 effector kinase Npr1.

(a) Left panel: During poor nitrogen supply, TORC1 activity is decreased via the GATOR1 complex including the Npr2 protein. Npr1 is active and enables S457 phosphorylation and activity of Mep2. Right panel: Upon glutamine supplementation, TORC1 is upregulated and Npr1 is downregulated. The Psr1 and Psr2 phosphatases enable dephosphorylation and thus inactivation of Mep2. This model does not discard an additional control of the activity of the Psr phosphatases by TORC1/Npr1 or other pathways. (b) Left panel: In the presence of poor nitrogen supply, the Npr1 kinase is active and enables S457 phosphorylation and silencing of the C-terminal autoinhibitory domain of Mep2. The enhancer C-terminal domain of Mep2 is free to activate the transport protein. The Psr1 and Psr2 phosphatases are also, at least partially, active in these conditions and mediate Mep2 dephosphorylation. Phosphorylated and non-phosphorylated Mep2 coexist in these conditions. Right panel: Upon glutamine supplementation, the Npr1 control is relieved and plasma-membrane Mep2 are rapidly dephosphorylated via the Psr phosphatases. The non-phosphorylated autoinhibitory domain of Mep2 prevents the enhancer domain to activate the transport protein.