Flurorcitrate resistant tricarboxylate transport mutants of Salmonella typhimurium.
Spontaneous and Tn10 induced fluorocitrate resistant mutants were isolated and characterized. These mutants were unable to grow on either cis-aconitate or DL-isocitrate but were still able to grow slowly on sodium citrate and normally on potassium or potassium-plus-sodium citrate. These mutants were defective in both citrate transport and citrate binding to priplasmic proteins. Tn10 insertion mutants were unable to produce immunologically detectable amounts of the citrate inducible periplasmic C protein previously shown to bind tricarboxylates. Using a series of tct::Tn10 directed Hfrs the tct locus was accurately positioned at 59 units between srlA and pheA, but was not cotransducible with either gene. In the absence of P22 mediated cotransduction with 16 adjacent chromosomal markers the srlA and tct loci were bridged by using a series of tct flanking Tn10 insertions, and by newly isolated and characterized nalB mutants. In addition the hyd and recA loci were located establishing the gene order in this region of the chromosome as: pheA tct nalB recA srlA hyd cys. Nitrosoguanidine derived tricarboxylate mutations (Imai 1975) were also mapped within the tct locus.[1]References
- Flurorcitrate resistant tricarboxylate transport mutants of Salmonella typhimurium. Somers, J.M., Sweet, G.D., Kay, W.W. Mol. Gen. Genet. (1981) [Pubmed]
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