FIGURE 4: Working model for interactions between the TOR pathway and tRNA modifications.

Loss of anticodon wobble uridine (U34) modifications enhances rapamycin sensitivity and NCR gene activation by Gln3 suggesting U34-minus mutants dampen TOR signaling. Such buffer function may operate upstream of TOR (1) or outside from TOR (2, 3) affecting steps that counter TOR-sensitive Gln3 inhibition. The latter (2, 3) may involve dephosporylation by a phosphatase (PPase) such as Sit4 (2) and/or Gln3 release from Ure2 (3) for mobilization and nuclear import. Alternatively, the effects of inappropriate U34 modifications on Gln3 misregulation could result from a combination of these options (1 – 3).

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