Fig. 11.

A proposed working model of TOR and CWI pathways medicated by the MoPpe1–MoSap1 complex. Thick lines indicate strengthened function, and thin lines indicate attenuated regulation. A. With abundant nutrients, the TOR signalling pathway is activated, leading to MoTap42 binding with MoPpe1 to inhibit its function while the phosphorylated MoNut1 remains cytoplasmic bound. The CWI pathway repression is caused by the dephosphorylation function MoPmp1 on CWI components. B. When treated with TOR specific inhibitor rapamycin or in nutrient starvation condition, TOR signalling was repressed. The activated MoPpe1–MoSap1 complex plays a dual role as a regulator to dephosphorylate MoNut1 and an activator of the CWI pathway through the strengthened repression on MoPmp1 and enhanced interaction with MoMkk1.