Over-expression of rexA nullifies T4rII exclusion in Escherichia coli K(lambda) lysogens

Dosage and relative cellular levels of RexA and RexB proteins encoded by the rexA-rexB genes of a lambda prophage are important for the Rex+ phenotype, which was nullified when greater RexA or RexB was provided than was necessary for the complementation of a rexA- or a rexB- prophage.     

Prophage lambda at unusual chromosomal locations. II. Mutations induced by bacteriophage lambda in Escherichia coli K12

An Escherichia coli strain deleted for the primary λ attachment site was lysogenized with λ at secondary sites. Some lysogens became mutants because of prophage insertion in the affected gene. Mutagenesis by phage λ is not random with respect to the gene affected: most mutants were pro, although certain other genes could be mutated at lower frequencies. In the case of several independent ilv and gal mutants, the sites of prophage insertion were in the same segment of the ilv region and galT gene respectively. The galT location may also be a preferred site for the insertion of DNAs other than prophage λ. Insertion of prophage λ within an operon can reduce the expression of operator-distal genes. A trpC λ insertion mutant expresses the operator-distal trpB function constitutively at a low level. This expression probably derives from a promoter located in the left arm of the prophage.     

Prophage substitution and prophage loss from superinfected Escherichia coli recA(P1) lysogens.

It is shown that the plasmid prophage P1 can be displaced by a superinfecting P1 phage in Escherichia coli recA(P1) lysogens. Six widely separated phage markers were used to distinguish between residual recombination and total substitution. It is further shown that superinfection of recA lysogens can lead to loss of both phage (curing). These two phenomena, previously reported in Rec+ strains, are thus independent of host recombination and may result from perturbations of some function involved in plasmid maintenance.     

Increased reproductive fitness of Escherichia coli lambda lysogens.

Lambda lysogens of Escherichia coli reproduce more rapidly than nonlysogens during aerobic growth in glucose-limited chemostats. If the environment is changed to anaerobic growth, the situation is reversed, and the lysogen reproduces more slowly than the nonlysogen. Based on a tetrazolium dye assay, the increased fitness of the lambda lysogen during aerobic growth seems to result from a continued high metabolic rate as glucose becomes limiting, whereas the metabolic rate of the nonlysogen declines. The lambda rex gene is required for the growth advantage of lysogens since lack of rex function causes lambda lysogens to lose their reproductive advantage over nonlysogens.     

Prophage induction in Escherichia coli K12 cells deficient in DNA polymerase I.

Summary The induction of prophage by ultraviolet light has been measured inE. coli K12 lysogenic cells deficient in DNA polymerase I. The efficiency of the induction process was greater inpolA1 polC(dnaE) double mutants incubated at the temperature that blocks DNA replication than inpolA ⁺ polC single mutants. Similarly, thepolA1 mutation sensitizedtif-promoted lysogenic induction in apolA1 tif strain at 42°. In strains bearing thepolA12 mutation, which growth normally at 30°, induction of the prophage occured after the shift to 42°. It is concluded that dissapearance of the DNA polymerase I activity leads to changes in DNA replication that are able, per se, to trigger the prophage induction process.     

Prophage Induction in Escherichia coli (Lambda) by N-Nitrosamines

Carcinogenic N-nitrosamines were tested for their ability to induce λ in a lysogenic strain of Escherichia coli K-12 (58-161 F⁺). Dimethylnitrosamine, di-n-propylnitrosamine, methyl-n-propylnitrosamine, and N-nitrosopiperidine were shown to be inducers of prophage.     

Induced radioresistance in four strains of Escherichia coli, two with lambda lysogens.

Cells of E. coli that are recA+ and lex+ show a phenomenon of induced radioresistance. A preexposure to ultraviolet light, or ionizing radiation followed by incubation to allow protein synthesis, followed by treatment with rifampin to prevent further induction, renders the cells resistant to further doses of radiation. When this is attempted with lambda lysogens of the same strains, no radioresistance is seen, even though the preexposure is too small to induce lambda itself. If the lysogens are ind-, namely lambda C1857, about the normal radioresistance can be developed by pretreatment. These findings suggest that the lambda repressors can bind to single-strand breaks caused by the inducing agent and can modify the course of induction.