Fig. 7.

Mechanism for the control of maltose uptake. A, Schematic model of the inducer exclusion mechanism. PTS permeases facilitate PTS sugar uptake into the cell. EIIA^glc is dephosphorylated, interacts with NBD and RD from different monomers of MalK, and is anchored to the inner leaflet of the membrane. The maltose transporter MalFGK₂ is thus trapped in an inactive conformation and maltodextrins uptake is inhibited. Consequently, maltodextrins (e.g. maltose, maltotriose) cannot further induce the maltose system by promoting the expression of malA and malB genes. B, Representation of the MalT positive regulation. In the absence of PTS sugars, the equilibrium of EIIA^glc is shifted towards its phosphorylated state (EIIA^glc-P) which cannot interact with MalK; therefore, transport can occur. Under these conditions, maltose induces the expression of malA and malB regions through its channeling into a metabolic pathway mediated by MalT-inducible enzymes. MalT is released from MalK and can be activated by (cognate) maltotriose imported or produced from the maltodextrin metabolism. MalT multimerization (upon its activation) allows its binding to the malA and malB promoters thereby inducing gene transcription. Of note, the divergent operon that belongs to the malA region and contains the malT gene is not shown, since it does not belong to the maltose regulon. Moreover, MalT-inducible operons located in other loci than malA and malB are also not shown for simplicity.