Figure 3.

SAM-responsive methylation of PP2a. (A) Under normal growth condition, when methionine and SAM are plentiful, PP2A is activated by methylation of its catalytic subunit by Ppm1p. Active PP2a dephosphorylates Npr2p, a component of the autophagy repressing complex SEACIT (SEAC subcomplex Inhibiting TORC1 signaling). Growth is promoted and autophagy is inhibited by active TORC1. (B) When methionine or SAM levels are low, PP2A is not methylated and therewith inactive, leading to hyperphosphorylated Npr2p. Under these conditions growth is repressed, TORC1 is inactive, and autophagy is promoted.