1887

Abstract

Two classes of pyridine nucleotide uptake mutants isolated previously in a strain of defective in both NAD biosynthesis () and pyridine nucleotide recycling () were analysed in terms of their genetic relationship to each other and their roles in the transport of nicotinamide mononucleotide as a precursor to NAD. The first class of uptake mutants, (99 units), failed to grow on nicotinamide mononucleotide (NMN) as a precursor for NAD. The second class, , grew on lower than normal levels of NMN and suppressed mutations. A third class of uptake mutant, , isolated in a background, also failed to grow on NMN. Transport studies and enzyme analyses confirmed these strains as defective in NMN uptake. A fourth locus, designated , was found to diminish NMN utilization in a background. Tn insertions near and were isolated and utilized in mapping studies. was found to map between and near . The locus was cotransducible with at 17 units while mapped at approximately 60 units. The biochemical and genetic data suggest that the and gene products cooperate in the utilization of NMN under normal conditions. A mutant, however, does not require the gene product for NMN uptake but does rely on the product. Fusion studies indicate that is regulated by internal NAD concentrations.

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/content/journal/micro/10.1099/00221287-131-6-1313
1985-06-01
2022-01-23
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