Fig. 5: Proposed working model for PhoP-dependent transcription regulation.

a The canonical RPo and three types of PhoP-dependent transcription activation in which PhoP exists as a tandem dimer, tetramer, and hexamer, respectively. b Classic transcription repression models by occluding RNAP binding sites at a promoter (upper panel) or locking RNAP on a promoter (lower panel). c A proposed “competitive occluding model” for PhoP-dependent transcription repression. In the absence of the upstream PhoP dimer, six GlnR molecules cooperatively and efficiently activate transcription of the target promoter. However, when the PhoP dimer interacts competitively with the a3’-b3’ sites and engages the adjacent GlnR molecules, these interactions cause significant distortion of the upstream DNA in the long spacer region, creating steric hindrances that impede the binding of a third GlnR dimer. Consequently, the formation and stabilization of a competent 6GlnR-TAC is disrupted, resulting in the repression of efficient GlnR-dependent transcription initiation. The repressor and spacer are represented as a five-pointed star and a rectangle, respectively, both colored in red.