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Fig. 1 | BMC Microbiology

Fig. 1

From: Relation between tetR and tetA expression in tetracycline resistant Escherichia coli

Fig. 1

TetR-tetA regulation model. Genetic organisation and mechanism of regulation of the Tn10-encoded tetracycline resistance determinant as proposed by Hillen and Berens [24]. The upper part of the figure describes processes occurring at the cytoplasmic membrane, while the lower part shows a schematic drawing of the genetic organisation and induction of the tetR and tetA genes. Tetracycline (tc) is assumed to enter the outer membrane by porins [1, 46]. The [tc · Mg]+ complex is formed, however it can dissociate and tetracycline can enter the cell by diffusion across the cytoplasmic membrane in its neutral form (middle). In the cytoplasm the [tc · Mg]+ complex is formed again. The same complex, indicated by triangles, is the molecular inducer of the Tet repressor (circles), encoded by tetR (thick grey arrow, bottom). TetR forms a dimer and binds to the two tandem tet operators O1 and O2 located between tetA and tetR in the absence of tetracycline. The genes have divergent polarities and are transcribed from overlapping promoters. When tetracycline is present, the [tc · Mg]+ complex binds to the TetR repressor-operator complex and triggers a conformational change in TetR so that it can no longer bind to the tet-operators, enforcing rapid dissociation from the DNA, enabling transcription of tetR and tetA (bottom, center). The [tc · Mg]+ complex is the substrate of the proton-tetracycline antiporter (TetA pump) which is indicated by its 12-α-helix membrane spanning structure. Modified from [9, 24]

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