SUMMARY: The enteric bacterium utilizes 1,2-propanediol as a sole carbon and energy source during aerobic growth, but only when the cells are also provided with cobalamin as a nutritional supplement. This metabolism is mediated by the cobalamin-dependent propanediol dehydratase enzyme pathway. Thirty-three insertion mutants were isolated that lacked the ability to utilize propanediol, but retained the ability to degrade propionate. This phenotype is consistent with specific blocks in one or more steps of the propanediol dehydratase pathway. Enzyme assays confirmed that propanediol dehydratase activity was absent in some of the mutants. Thus, the affected genes were designated (for defects in utilization). Seventeen mutants carried pdu:: lac operon fusions, and these fusions were induced by propanediol in the culture medium. All of the mutations were located in a single region (41 map units) on the chromosome between the (histidine biosynthesis) and branch I (cobalamin biosynthesis) operons. They were shown to be P22-cotransducible with a branch I marker at a mean frequency of 12%. Mutants that carried deletions of the genetic material between and also failed to utilize propanediol as a sole carbon source. Based upon the formation of duplications and deletions between different pairs of :: Mu dA insertions, the genes were transcribed in a clockwise direction relative to the genetic map.


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