Figure 10.

Simplified model representing key molecular actors involved in the competition for sugars at the A. thaliana/B. cinerea interface. Upon infection by B. cinerea, unloaded sucrose is mainly cleaved into glucose and fructose. Cell wall invertases from host (AtCWIN1) contribute to the accumulation of hexoses in the apoplast through transcriptional and posttranslational regulations. Host cells can assimilate free hexoses via the induced activity of hexose-specific transporters belonging to the Sugar Transporter Protein (STPs) family. B. cinerea possesses its own functional sucrolytic machinery (Bc1g10247 ?) and also a multigenic hexose uptake system (BcHXTs and BcFRT1). A secondary pathway for apoplastic sucrose retrieval involving sucrose transporter has been evidenced. Intracellular sucrolytic machinery, involving VINs and to lesser extent CINs, is efficient to provide intracellular hexoses to maintain sugar homeostasis in host cells and to fuel plant defenses. The precise regulatory role of tonoplastic, plasma membrane sucrose transporters and sugar facilitators (SWEETs) needs to be elucidated.