Genes for l-sorbose utilization in Escherichia coli.
Amongst forty wild strains of Escherichia coli, nine used L-sorbose as a source of carbon and energy and two mutated to use it. Laboratory strains K12, B and C were L-sorbose-negative. Genes for L-sorbose utilization (sor+) were transferred to K12 from six wild strains; genes conferring the mutable phenotype were also transferred. All were cotransducible with metA at 90 min on the linkage map. The most probable gene order was met ace sor pgi mal. Complementation tests identified two genes for L-sorbose utilization. Genetical evidence showed that the catabolite repressor protein of K12 exerted positive control over sor+ genes introduced into K12. The genes for phosphofructokinase ( pfkA), the phosphocarrier protein (ptsH) and phosphotransferase enzyme I ( ptsI) were required for utilization of L-sorbose. The frequency of transduction of sor+ was low when selection was made for sor+, because L-sorbose partially inhibited the growth of both L-sorbose-negative strains and K12 (sor+) strains. Uridine, thymidine and sorbitol each annulled the inhibition of growth and increased the frequency of transduction of sor+.[1]References
- Genes for l-sorbose utilization in Escherichia coli. Woodward, M.J., Charles, H.P. J. Gen. Microbiol. (1982) [Pubmed]
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