Phosphoribosyl diphosphate synthetase-independent NAD de novo synthesis in Escherichia coli: a new phenotype of phosphate regulon mutants.
Phosphoribosyl diphosphate-lacking (delta prs) mutant strains of Escherichia coli require NAD, guanosine, uridine, histidine, and tryptophan for growth. NAD is required by phosphoribosyl diphosphate-lacking mutants because of lack of one of the substrates for the quinolinate phosphoribosyltransferase reaction, an enzyme of the NAD de novo pathway. Several NAD-independent mutants of a host from which prs had been deleted were isolated; all of them were shown to have lesions in the pstSCAB-phoU operon, in which mutations lead to derepression of the Pho regulon. In addition NAD-independent growth was dependent on a functional quinolinate phosphoribosyltransferase. The prs suppressor mutations led to the synthesis of a new phosphoryl compound that may act as a precursor for a new NAD biosynthetic pathway. This compound may be synthesized by the product of an unknown phosphate starvation-inducible gene of the Pho regulon because the ability of pst or phoU mutations to suppress the NAD requirement requires PhoB, the transcriptional activator of the Pho regulon.
Hove-Jensen
B
B
Department of Biological Chemistry, University of Copenhagen, Denmark.
D004926:Escherichia coli / Q000378:metabolism*; D009154:Mutation; D009243:NAD / Q000096:biosynthesis*; D009537:Nicotinamide Mononucleotide / Q000378:metabolism; D010641:Phenotype; D010754:Phosphoribosyl Pyrophosphate / Q000172:deficiency; D012268:Ribose-Phosphate Pyrophosphokinase / Q000502:physiology*
D009243:NAD; D009537:Nicotinamide Mononucleotide; D010754:Phosphoribosyl Pyrophosphate; D012268:Ribose-Phosphate Pyrophosphokinase