FIG. 7.
Stabilization of ZntR and its effect on zinc homeostasis. (A) Model of cooperative ZntR stabilization by zinc and DNA. Apo-ZntR is unstable, and addition of zinc enhances ZntR t1/2 in a DNA-dependent manner. (B) Regulated degradation of ZntR contributes to zinc homeostasis in E. coli through a feedback loop. At low intracellular zinc levels, apo-ZntR is unstable and leads to lack of zinc export due to poor activation of zntA transcription. Lack of zinc export and activation of zinc import result in high intracellular zinc concentrations. ZntR binds zinc, and the zinc-bound form of ZntR is more stable and strongly activates zntA transcription. This change leads to high efflux of zinc and inactivation of zinc uptake, which closes the feedback loop with a low zinc concentration in the cell.