Figure 7

Model of the sugar competition between Arabidopsis cells and Botrytis cinerea. Upon infection, secreted PAMPs and/or host-derived signals (DAMPs) are recognized by PRRs, resulting in a transcriptional reprogramming of host sugar transporters. Putative fungal effectors may also manipulate host SWEET gene expression. Apoplastic sucrose is cleaved into glucose and fructose by cell wall invertases which can originate from both the host (AtCWIN1) and/or the pathogen (BcCWINs). Arabidopsis and Botrytis compete for free hexoses through specific activities of sugar transporters (BcHXTs and BcFRT1 for B. cinerea) which have differential specificity and affinity for hexoses. On the plant side, the Botrytis-induced sugar uptake activity is accompanied with a reduction of internal sugars and an increased O2 consumption suggesting an enhanced activity of the glycolysis and the cellular respiration. Together, these changes in host primary metabolism may contribute to deprive the pathogen from sugar resources and to fuel plant defence responses.