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　　A schematic model of the different roles of plant sugar transporters in response to pathogen infection and the involvement of microbial INV and sugar transporters in plant–pathogen interactions. Clade II and III SWEETs export Glc and Suc into the plant apoplasm, respectively. Glc is then directly taken up into bacteria and necrotrophic/hemibiotrophic fungi during the initial infection phase via their own plasmalemma-localized hexose transporters (HXT), whereas Suc is first hydrolyzed into Glc and Fru by plant CWIN or pathogen-secreted INV before being imported into the pathogen cells. Consequently, these SWEETs promote bacterial and necrotrophic/hemibiotrophic fungal growth in the apoplasm. By contrast, Clade I SWEETs can sequester cytosolic Glc into plant cell vacuoles, thereby reducing the availability of Glc in the apoplasm, which starves necrotrophic fungi. The plant STPs facilitate hexose uptake into plant cells, which is subsequently released into the extrahaustorial matrix (EHMx) for uptake by biotrophic fungi via fungal HXT, thus promoting fungal infection. On the other hand, STPs reduce the concentration of Glc at the apoplasm, which inhibits the development of bacteria and necrotrophic/hemibiotrophic fungi. Plant SUTs take up apoplasmic Suc into plant cells and are commonly induced by pathogen infection. Studies in mycorrhizal fungi indicate that SUT (i) may promote the development of biotrophic fungi through increasing the intracellular sugar pool for subsequent import to the EHMx and uptake by Suc transporters such as UmStrt1, and (ii) could inhibit the development of bacteria and necrotrophic/hemibiotrophic fungi by limiting Suc availability in the apoplasm of the plant cell. NB, neckband.