Sentence examples for competitive defects from inspiring English sources

In addition to the PrfA*-related metabolic shift of L. monocytogenes towards glycerol utilization, our data indicate that the competitive defects exhibited by prfA* mutants in broth culture were exacerbated under conditions of osmotic and/or acid stress (Fig. 3).

Although no dramatic differences were observed for mutant and wild type strains with respect to growth in monoculture (Fig. 3AC), the prfA G155S mutant and the prfA G145S mutant exhibited more severe competitive defects when mixed with the wild type strain and grown in BHI supplemented with 5% NaCl in comparison to BHI lacking additional NaCl (Fig. 3B).

Examination of the fitness of prfA* ΔsigB double mutant strains in BHI indicated that the double mutant exhibited a competitive defect that was approximately equivalent to the sum of the competitive defects exhibited by the prfA* and ΔsigB single mutants (Fig. 4).

The findings further indicate that competitive defects associated with the prfA* strains in other media cannot simply be attributed to the metabolic burden of increased PrfA-dependent gene product expression, as high expression levels are maintained by prfA* strains in the presence of glycerol ([44], [45] and J. Bruno, unpublished).

The presence of glucose thus exacerbated the competitive defect associated with PrfA activation in broth culture.

The prfA G145S mutant exhibited a similarly exacerbated competitive defect under acid stress.

When mixed cultures of wild type and prfA G145S bacteria were grown under these conditions, the resulting competitive defect was essentially identical to the competitive defect observed for mixed cultures grown to stationary phase (Fig. 1D).

Therefore, the stress related competitive defect associated with the constitutive activation of PrfA appears distinct from the defect associated with the loss of SigB function.

Interestingly, the magnitude of the competitive defect exhibited by the ΔsigB mutant closely resembled that observed for prfA G145S mutants in BHI (Fig. 4C).

To determine if the competitive defect associated with prfA* strains was related to an impairment of SigB function, prfA G155S ΔsigB and prfA G145S ΔsigB double mutants were tested in broth competition assays.

A direct correlation thus appeared to exist between the level of PrfA activation conferred by a prfA* mutation and the magnitude of the competitive defect observed in broth culture.