FIG 8.

Proposed model for RpoN-dependent susceptibility to TOB+FUM. (Left) In the wild-type RpoN⁺ strain, FUM enters the cell through C₄-dicarboxylate transporters (e.g., DctA) that are transcriptionally regulated by RpoN. Once in the cell, FUM is metabolized in the TCA cycle to produce reducing equivalents that promote ETC activity. Increased respiration leads to regeneration of the membrane potential, TOB uptake, and subsequent TOB-dependent cell death. (Right) On the other hand, in the ΔrpoN RpoN⁻ strain, the lack of functional RpoN means that C₄-dicarboxylate transporters are not expressed, and FUM cannot enter the cell. As a consequence, TOB uptake is not increased, and the cell remains tolerant to TOB.