[Isolation of Escherichia coli K-12 mutants that affect the development of phage phi m173 (imm phi 80)]. / Vydelenie mutantov Escherichia coli K-12, vliiaiushchikh na razvitie faga fi m173 (imm fi 80).

Escherichia coli mutants which block the development of a number of lambdoid phages, particularly, phi m173 and phi 80 were selected. These mutants have different phenotypes, being resistant to different groups of lambdoid phages. There are also differences between new mutants and gro mutants of E. coli studied earlier. The results obtained support the suggestion that no replication of different lambdoid phages takes place in these mutants.

[Isolation and genetic analysis of bacterial mutations gpr blocking the replication of various lambda phages]. / Vydelenie i geneticheskoe izuchenie bakterial'nykh mutatsii gpr, blokiruiushchikh replikatsiiu nekotorykh liambdoidnykh fagov.

Bacterial mutations affecting phi 80 DNA replication have been isolated and designated gpr2, 27. The main difference between gpr2, 27 and groP, grp mutations described earlier is that mutations gpr2, 27 are not essential for lambda replication. The mutations have been mapped between thr and leu loci in the vicinity of mutations groPC756 (dnaK gene) and groPC259 (dnaJ gene), their order being: thr-gpr2-groPC756-groPC259-gpr27. Complementation analysis using transducing phages suggested that mutations gpr2, 27 are localized in genes unknown earlier, outside dnaK and dnaJ genes.

[Cloning and complementation analysis of the Escherichia coli gpr locus, influencing DNA replication of certain lamdoid phages]. / Klonirovanie i komplemntatsionnyi analiz lokusa gpr Escherichia coli, bliiaiushchego na replikatsiiu DNK nekotorykh liambdoidnykh fagov.

Escherichia coli DNA fragments which suppressed gpr27 and gpr2 mutations in the earlier proposed gprA and gprB genes, respectively, were cloned within phage vectors. Mutations gpr2 and gpr27 restrict DNA replication of some lambdoid phages and are located in the region of dnaK, J genes. DNA-DNA hybridization showed that the cloned fragments correspond to the region where gpr mutations were genetically mapped and, in some cases, do not include dnaK, J genes. These results provide the evidence that gprA and gprB genes may be physically separated from dnaK, J genes.