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PubMed1979

Enzymatic degradation of uracil-containing deoxyribonucleic acid. V. Survival of Escherichia coli and coliphages treated with sodium bisulfite.

A number of mutants of Escherichia coli defective in the ung gene (structural gene for uracil-deoxyribonucleic acid [ura-DNA] glycosylase) are shown to be abnormally sensitive to treatment with sodium bisulfite when compared with congenic ung+ strains. These results provide further evidence that sodium bisulfite causes the deamination of cytosine to uracil in DNA and that ura-DNA glycosylase is required for the repair of U-G mispairs. The effect of the chemical is apparently selective with respect to base damage; coliphages containing cytosine in their DNA are inactivated by treatment with sodium bisulfite, whereas those containing hydroxymethylcytosine are not. ura-DNA glycosylase and the major apurinic-apyrimidinic endonuclease of E. coli may function in the same repair pathway, since the extent of inactivation of a congenic set of strains which are ung xth (structural gene for the major apurinic-apyrimidinic endonuclease of E. coli) or ung xth+ is the same.

Biodegradation, Environmental↗
PubMed1983

Coliphage P1-mediated transduction of cloned DNA from Escherichia coli to Myxococcus xanthus: use for complementation and recombinational analyses.

We have found that coliphage P1 can be used to transduce cloned DNA from Escherichia coli to Myxococcus xanthus. Transduction occurred at a high efficiency, and no evidence for DNA restriction was observed. The analysis of the transductants showed that they fall into three general categories: (i) haploid cells which contain portions of the cloned DNA substituted for homologous chromosomal DNA; (ii) heterozygous merodiploids which contain the recombinant plasmid integrated into the chromosome at a region of homology; and (iii) homozygous merodiploids which contain two copies of a portion of the cloned DNA with the loss of the chromosomal copy of the genes. The merodiploids, once formed, are relatively stable. They were used to analyze two genes necessary for aggregation and thus fruiting body formation. P1 transduction also permits the reintroduction and substitution of mutated regions of cloned DNA into M. xanthus for the analysis of the role of the DNA in cellular physiology and development.

Cloning, Molecular↗
PubMed1993

Genes for the establishment and maintenance of lysogeny by the temperate coliphage 186.

To identify the genes in coliphage 186 that are required for lysogeny, we isolated clear-plaque mutants. Complementation studies and DNA sequencing identified two genes, the cI gene for the immunity maintenance repressor and the cII gene, which is required only for the establishment of lysogeny. One mutant carried a change in the LexA-binding site controlling expression of the antirepression protein Tum.

Bacterial Proteins↗
PubMed1996

Analysis of the enzymatic cleavage (beta elimination) of the capsular K5 polysaccharide of Escherichia coli by the K5-specific coliphage: reexamination.

The capsular K5 polysaccharide of Escherichia coli is the receptor of the capsule-specific coliphage K5, which harbors an enzyme that degrades the capsular K5 polysaccharide to a number of oligosaccharides. Analysis of the degradation products using gel permeation chromatography, the periodate-thiobarbituric acid and bicinchoninic acid reactions, and nuclear magnetic resonance spectroscopy showed that the major reaction products are hexa-, octa-, and decasaccharides with 4,5-unsaturated glucuronic acid (delta4,5GlcA) at their nonreducing end. Thus, the bacteriophage enzyme is a K5 polysaccharide lyase and not, as we had reported previously, an endo-N-acetylglucosaminidase.

Bacterial Capsules↗
PubMed1996

Proteins responsible for lysogenic conversion caused by coliphages N15 and phi80 are highly homologous.

Lysogenic conversion caused by lambdoid bacteriophage phi80 and that caused by coliphage N15 have similar characteristics, suggesting that similarities in their cor genes and Cor proteins are responsible for this effect. Here we present the nucleotide sequence of the N15 cor gene. The N15 cor gene homolog was found in the phi80 cor region, but in the opposite direction of that of the open reading frame to which the phi80 cor gene had previously been assigned (M. Matsumoto, N. Ichikawa, S. Tanaka, T. Morita, and A. Matsushiro, Jpn. J. Genet. 60:475-483, 1985).

Amino Acid Sequence↗
PubMed2001

Establishing lysogenic transcription in the temperate coliphage 186.

A single-copy chromosomal reporter system was used to measure the intrinsic strengths and interactions between the three promoters involved in the establishment of lysogeny by coliphage 186. The maintenance lysogenic promoter p(L) for the immunity repressor gene cI is intrinsically approximately 20-fold weaker than the lytic promoter p(R). These promoters are arranged face-to-face, and transcription from p(L) is further weakened some 14-fold by the activity of p(R). Efficient establishment of lysogeny requires the p(E) promoter, which lies upstream of p(L) and is activated by the phage CII protein to a level comparable to that of p(R). Transcription of p(E) is less sensitive to converging p(R) transcription and raises cI transcription at least 55-fold. The p(E) promoter does not occlude p(L) but inhibits lytic transcription by 50%. This interference is not due to bound CII preventing elongation of the lytic transcript. The p(E) RNA is antisense to the anti-immune repressor gene apl, but any role of this in the establishment of lysogeny appears to be minimal.

Coliphages↗
PubMed1966

Inhibition of coliphage reproduction after superinfection of induced lysogens.

Brenner, Don J. (University of Washington, Seattle), and Neal B. Groman. Inhibition of coliphage reproduction after superinfection of induced lysogens. J. Bacteriol. 92:1727-1734. 1966.-Purified preparations of phages lambda and lambda112 inhibited lysis, phage reproduction, and endolysin synthesis by ultraviolet-induced strains of K-12 (lambda) and K-12 (lambda112). Structural and partial functional integrity of phage was required for inhibition, and the role of phage deoxyribonucleic acid (DNA) in inhibition was demonstrated. Both ultraviolet-irradiated and host-modified lysates of lambda were inhibitory, suggesting that replication of superinfecting phage DNA was not essential for inhibition. Using various combinations of superinfecting and resident phage, including lambda, 434, 434hy, and C-mutant derivatives, we observed that all three C region cistrons played some role in inhibition. Of the three, the C(1) cistron was the most critical. With certain phage combinations, inhibition was observed even though the resident and superinfecting phage differed in immune specificity. Both the medium and the method of superinfection determined whether lysis or lysis inhibition would occur. These and other observations with K-12(lambda)thy(-) indicated that many factors influence the outcome of superinfection. The data are compatible with the view that superinfection inhibition is due to the establishment or re-establishment of phage repressor activity, with the result that replication of both superinfecting and resident phage is blocked.

Antibodies↗
PubMed1967

Susceptibility of different coliphage genomes to host-controlled variation.

Twenty-eight coliphages were studied for their susceptibility to four systems of host control variation in Escherichia coli. Both temperate and virulent phages were studied, including phages with ribonucleic acid, double- and single-stranded deoxyribonucleic acid (DNA) and glucosylated DNA. The systems examined were E. coli C-K, K-B, B-K, and K-K(P1). The C-K, K-B, and B-K systems affected temperate phages and nonlysogenizing mutants derived from temperate phages. In general, these systems did not restrict virulent phages. Phage 21e, a variant of phage 21, lost the ability to undergo restriction in the C-K and B-K systems, but retained susceptibility to the K-B and K-K(P1) systems. This suggests that the genetic site(s) on the phage, as well as in the host, determines susceptibility to host-controlled variation. Both temperate and dependent virulent phages were susceptible to the host control system resulting from the presence of prophage P1. The autonomous and small virulents were not susceptible. In a given system, the various susceptible phages differed widely in their efficiency of plating on the restricting host. If the few infections that occur arise in rare special cells, then different populations of special cells are available to different phage species. For most phage types, when a susceptible phage infected a nonrestricting host, the progeny showed the specificity appropriate to that host. Behavior of T3 was exceptional, however. When T3 obtained from E. coli K infected E. coli C or B, some of the progeny phages retained K host specificity, whereas others acquired the specificity of the new host.

Bacteriolysis↗
PubMed1972

Behavior of coliphage lambda in Shigella flexneri 2a.

The insensitivity of wild-type Shigella flexneri 2a to coliphage lambda is a consequence of its native genetic defect in the malA gene cluster. The "smooth" S. flexneri 2a lipopolysaccharide layer affects the efficient adsorption of lambda. Derivatives, capable of serving as functional hosts for lambda, were obtained by repairing the malA lesion, enabling the expression of the malB-lambdarcp region of S. flexneri. Introduction of a mutation into S. flexneri causing a "rough" lipopolysaccharide character resulted in more efficient adsorption of lambda. Such S. flexneri hosts can be stably lysogenized and upon induction yield gal(+)-transducing lysates. Lambda propagated on a malA(+) rough S. flexneri host was restricted by Escherichia coli K-12 and E. coli B, but not by E. coli C. This S. flexneri host did not restrict lambda grown on these E. coli strains.

Adsorption↗
PubMed1973

Transduction of Gal+ by coliphage T1. 3. Requirement for transcription and translation in recipient cells.

A 10- to 15-min derepression of a lambda prophage in a Gal(-) recipient during early infection with a transducing lysate of coliphage T1am will cause an increase in the efficiency of transduction of Gal(+). An increase in the efficiency of transduction occurs when the donor is either nonlysogenic or lysogenic for lambda; the increase is blocked by rifampin or chloramphenicol. With strain R901 it has been shown that efficient transduction can be blocked by treatment with rifampin after all chloramphenicol-sensitive steps have occurred.

Chloramphenicol↗
PubMed1974

Localization of coliphage MS2 A-protein.

The purification of coliphage MS2 dinitrophenol (DNP) conjugates provided a system for localization of the single molecule of A-protein in the capsid of the MS2 phage particle. Three A-protein preparations isolated from unconjugated MS2, overconjugated DNP-MS2, and purified 78S DNP-MS2 were tested for the presence of covalently bound DNP. The binding characteristics to Dowex 1-X8 and rabbit anti-DNP bovine serum albumin (DNP-BSA) immunoglobulin G of the 78S DNP-MS2 and overconjugated DNP-MS2 A-protein preparations indicate that the A-protein is located on the surface of the phage particle where it can be covalently conjugated with hapten. Extensive enzymatic iodination of the A-protein of intact unconjugated MS2 substantiates this conclusion.

Coliphages↗
PubMed1975

Effect of UV irradiation on transduction by coliphage T1.

Lysates of the virulent coliphage T1 transduce seven markers between strains of Escherichia coli with reproducilble efficiencies which range from 10(-7) to 10(-5). The ability of a UV-irradiated lysate to transduce Arg(+), Str(R), Trp(+), Lac(+), and Pro(+) is 90% and Bio(+) is 99% inactivated by doses which inactivate plaque formation of T1 by six orders of magnitude. A dose of irradiation which causes a 1- to 2-log drop in the titer of T1 stimulated Gal(+) transduction by two- to three-fold; no other marker tested was stimulated. Irradiation causes dislinkage of some co-transducible markers but not others.

Arginine↗
PubMed1975

Genetic studies of coliphage P1. I. Mapping by use of prophage deletions.

One hundred and ten amber mutants of coliphage P1 were isolated and localized into groups with respect to the existing genetic map by use of nonpermissive Escherichia coli K-12 strains lysogenic for P1 with deletions. These lysogens contain one of three types of deletion prophages: P1cry and its derivatives, P1dlacs, and P1dpros. Fourteen such lysogens were tested for their ability to rescue the amber mutants which were then assigned to one of nine deletion segments of the P1 genome defined by the termini of the various prophage deletions. The relationship of the nine deletion segments with the published P1 map is described, two new segments having been added. The deletions of the 14 prophages overlapped sufficiently to indicate that the P1 genetic prophage map should be represented in circular form, which is consistent with the fact that P1 is normally a circular plasmid in the prophage state. The distribution of mutants into deletion segments is nonrandom for at least one segment. In addition, the deletion termini of the 14 defective prophages coincided in five out of nine regions separating the nine deletion segments. Various possible explanations are discussed for the nonrandom recurrence of these deletion termini, including the evidence of hot spots of recombination.

Alleles↗
PubMed1976

Genetic studies of coliphage P1. III. Extended genetic map.

An extensive genetic map of coliphage P1 has been constructed for 113 amber mutants, using primarily a modification of the conventional complementation spot test. These spot tests failed to classify the mutants into cistrons, but when they were quantitated they permitted assignment of the mutants into 10 linkage clusters. Furthermore, a linear order could be deduced for most of the mutants within each cluster. This strongly suggested that recombination was the predominant event generating plaques and that, for the practical purpose of rapid genetic mapping, such spot tests could be considered as a series of two-factor crosses. Six of the 10 linkage clusters correlated with the P1 genetic map established by Scott (1968). The locations of the remaining four clusters were determined by three-factor crosses and by prophage deletion mapping. The nonrandom occurrence of termini for 14 deletion prophages, which we established previously (Walker and Walker, 1975), and the coincidence of these termini with five out of ten regions demarcating the linkage clusters are discussed. Complementation tests in liquid frequently gave ambiguous results. Therefore, cistron designations were not assigned.

Chromosome Mapping↗
PubMed1969

Serological relatedness of the ribonucleic acid-containing coliphages.

The serological relationship of the ribonucleic acid (RNA)-containing coliphages MS-2, M-12, R-17, f(2), beta, fr, f(4), and Qbeta was determined. Antisera against MS-2, R-17, f(2), fr, and Qbeta neutralized the infectivity of all of these RNA phages to varying degrees. Although each phage was serologically distinct, the antisera cross-reacted with certain phages to approximately the same degree, indicating the antigenic relationship of the coat proteins of these phages. Adsorption of anti-MS-2 sera with varying concentrations of all of the phages demonstrated that these viruses contain similar yet unique antigenic determinants. It is suggested that these RNA phages are mutants of two related phages rather than of the same phage.

Antigen-Antibody Reactions↗
PubMed1981

Coliphage 186 Replication is delayed when the host cell is UV irradiated before infection.

In contrast to results with injections by lambda and P2, the latent period for infection by coliphage 186 is extended when the host cell is UV irradiated before infection. We find that 186 replication is significantly delayed in such a cell, even though the phage itself has not been irradiated. In contrast, replication of the closely related phage P2 under the same conditions is not affected.

Bacteriophage lambda↗
PubMed1981

Coliphage 186 infection requires host initiation functions dnaA and dnaC.

We show that coliphage 186 infection is dependent upon host initiation functions, dnaA and dnaC, which differentiates the phage from lambda and P2. The possibility is therefore entertained that the delay in 186 replication seen after infection of UV-irradiated bacterial cells reflects the temporary unavailability of one or both these functions. Infections with P1 and Mu need host dnaC but not dnaA and show some sensitivity to preirradiation of the host but are not as sensitive as 186.

Coliphages↗