[Genetic study of Escherichia coli K-12 mutants resistant to 2,6-diaminopurine].
Mutants, resistant to the inhibitory effect of 2,6-diaminopurine and incapable of utilizing adenine as a purine source, are obtained from purinenucleoside phosphorylase-defective purine-dependent Escherichia coli K-12 strains. The mutations obtained (apt) disturb the uptake of adenosine and inosine only in the presence of a mutation for purinenucleoside phosphorylase (pup gene) in the genome of purine-dependent bacteria. The introduction of pup+ allele into the genome of mutants obtained (genotype purDpup apt) results in the restoration of the ability to uptake adenine and purine ribosides. Strains of purDpup+apt genotype are characterized by more short generation time under the growth in the presence of adenine as compared with purDpup apt+ strains which indicates the existance of an efficient pathway of adenine utilization in E. coli with the cooperation of purinenucleoside phosphorylase. Mutations apt have revealed a combined transfer with purE marker under the transduction frequency of approximately 5%. The gene order on E. coli K-12 chromosome is apt-purE-gal, as estimated from the data on conjugation crosses.
D004352:Drug Resistance, Microbial; D004926:Escherichia coli / Q000187:drug effects*; D009154:Mutation; D011687:Purines / Q000494:pharmacology*
D011687:Purines
Geneticheskoe izuchenie mutantov Escherichia coli K-12, ustoĭchivykh k 2,6-diaminopurinu