Figure 4. The increased susceptibility of prfA* cultures to stress is unrelated to sigB function.

(A) Rationale regarding how the competitive defect exhibited by a prfA* ΔsigB double mutant can be used to determine if the competitive defect associated with constitutive PrfA activation is related to an impairment of SigB function. If constitutive activation of PrfA (PrfA*) impairs SigB function, the magnitude of the competitive defect exhibited by a prfA* ΔsigB double mutant strain will be equivalent to the magnitude of the competitive defects exhibited by the prfA* and ΔsigB single mutants. If constitutive activation of PrfA (PrfA*) does not impair SigB function, the magnitude of the competitive defect exhibited by a prfA* ΔsigB double mutant will be equivalent to the sum of the magnitudes of the competitive defects exhibited by the prfA* and ΔsigB single mutants. (B) Assessment of the competitive index for the prfA G155S ΔsigB double mutant. The wild type cam^R strain was mixed with a chloramphenicol-sensitive test strain in BHI at 37°C. Mixed cultures were subjected to repeated cycles of growth and dilution (1∶100) into fresh BHI every 24 hours, and CI values were determined immediately prior to each dilution. The data represent the means ± standard errors of two independent experiments. (C) Assessment of the competitive index for the prfA G145S ΔsigB double mutant. The wild type cam^R strain was mixed with a chloramphenicol-sensitive test strain in BHI at 37°C. Mixed cultures were subjected to repeated cycles of growth and dilution (1∶100) into fresh BHI every 24 hours, and CI values were determined immediately prior to each dilution. The data represent the means ± standard errors of two independent experiments.