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. 2018 Oct 19;8:15509. doi: 10.1038/s41598-018-33647-w

Figure 9.

Figure 9

Suggested model for the regulation of extracellular ADPG uptake and utilization in E. coli in the mammalian intestine. According to this model, NupC and NupG, as well as the integrity of the outer membrane (OM), act as major determinants of the process. Under conditions of glucose (primary carbon source) limitation, augmented cAMP levels and concomitant activation of CRP will enhance the expression of nupC and nupG, thus favoring the scavenging of extracellular ADPG. These conditions will also enhance the expression of pathways involved in the catabolism of mono- and disaccharides derived from the degradation of complex polysaccharides by the intestine microbiota. It is conceivable that the OM of E. coli will be periodically damaged by bile acids and other membrane-damaging substances and conditions occurring in the intestine, allowing passive diffusion of ADPG molecules into the periplasm and access to the inner membrane NupC and NupG transporters. In the cytoplasm, the scavenged ADPG is employed to produce glycogen and ADP by GlgA, the former used as a carbon and energy storage compound for survival and colonization2,29 and the latter to fuel purine nucleotides metabolism (this work).