Results and Discussion
A S. Typhimurium ∆pagR strain grows poorly with succinate as a sole carbon and energy source­ . We probed for areas ofS. Typhimurium metabolism that might be regulated by PagR. To this end, we tested the ability of a S. TyphimuriumpagR1::kan + strain to catabolize various carbon sources. During this screen, we observed that apagR1::kan + strain (JE21566) struggled to grow when succinate was the sole carbon and energy source (Fig. 2A, gray triangles vs red circles). The observed phenotype was solely due to the lack of PagR, since we restored growth to the rate and cell density of a culture of the pagR + strain by ectopically expressing the pagR + allele (Fig. 2A, dark green triangles). Surprisingly, we also corrected the growth phenotype by deleting the tktD and tktE genes encoding the two subunits of the TktC transketolase (tktDE1 ::cat+ , Fig. 2A, blue squares). The latter was a notable result because the correction of the phenotype was as efficient as the ectopic expression ofpagR +. Conversely, the ectopic expression of the tktDE + genes repressed growth (Fig. 2B, magenta squares), mimicking the growth behavior of apagR1 ::kan+ strain (Fig. 2B, gray triangles). We wanted to learn whether the phenotype observed when thetktDE + genes were overexpressed was a result of having excess transketolase activity or whether TktC, was somehow different to TktA and TktB. For this purpose we expressed the other twoS. Typhimurium transketolases in thepagR1 ::kan+tktDE1 ::cat+ strain and monitored cell growth. Neither the ectopic expression of tktA+ nortktB+ repressed the growth of thepagR1 ::kan+tktDE1 ::cat+ strain (Fig. 2B, light green squares and yellow squares vs magenta squares). Rather, expression of tktA+ andtktB+ improved growth relative to the vector control. From these results we learned that the cell could not overcome whatever the deleterious effect of having TktC in excess was when growing on succinate.