Figure 1.

Model for the regulation of autophagy in Arabidopsis seedlings under sugar starvation and sugar excess. The model represents three conditions, (i) sugar starvation, (ii) normal (unstressed) growth conditions, (iii) high sugar levels and/or stress conditions. (i) Low T6P levels activate sugar starvation-based autophagy, by rendering SnRK1 active. Active SnRK1 in turn inhibits TOR, activating autophagy. (ii) Suc is broken down to sugars and sugar phosphates by Suc synthase (SuSy) and invertases (INV). When these Suc-splitting enzymes (Susy/INV) are readily able to deal with Suc, T6P is synthesized by TPS and TPP, its level mirroring Suc levels. T6P inhibits SnRK1 which on its turn inhibits TOR-kinase, an inhibitor of autophagy. (iii) Excess sugar levels (excessive import, exogenous sugar supply) can probably also induce autophagy, at least partly through stimulating ABA synthesis and signaling the SnRK2/TOR nexus. Suc can also be metabolized in the apoplast by cell wall INV (cwINV), producing free Glc and Fru. Normally, these hexoses are rapidly imported by sugar transport proteins (STP) and used for growth associated with TOR signaling. Under stress, growth is compromised, leading to reduced uptake and increased extracellular Glc which can be sensed by the Regulator of G-protein signaling (RGS1), in turn activating autophagy through an unknown mechanism. Red blunt arrows indicate negative regulation and green arrows positive regulation. Dashed lines represent potential regulatory mechanisms. Enzymes are indicated in blue. Mechanisms that are not active during a specific condition are faded.