Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Coliphages”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 577 records · Page 32Linked to original sources
PubMed1976

Effects of the phage P1 restriction system on coliphage phi W: degradation and complex formation of phage phi W DNA.

Growth of phages phi W and T7 was restricted in Escherichia coli lysogenic for phage P1. Only a fraction of the infected cells gave burst of phages. Cells permitting phage growth gave normal burst size. Host strains carrying P1 mutants with defective endonuclease gave no restriction of phages T7 and phi 3, the latter a host-range mutant of phi W. Degradation but not modification of parental phage DNA could be demonstrated. Although no DNA, RNA or protein was synthesized in phi W infected P1 lysogenic cells, the parental phage DNA was found in increasingly larger complexes during the course of infection. At early times after infection, parental phage DNA was found to sediment about twice as fast as mature phage DNA. At later times during the infection the parental phage DNA was recovered as a very rapidly sedimenting material. Such material was also found in alkaline sucrose gradient centrifugation after treatment of the cell extract with sodium dodecyl sulphate, pronase digestion and phenol extractions.

Coliphages↗
PubMed1976

Transcriptional control of T4 coliphage-specific genes 30, 42, 43, rIIA, rIIB, and e.

Escherichia coli B/r (suo) was infected, at 30 degrees C, with T4Dam+, T4DamB24-amN82 (I-, 44-, DNA-negative phenotype), and T4DamN134amBL292 (33-, 55-, maturation-defective phenotype). A genetic ('transformation') assay was used to monitor transcription of genes 30 (polynucleotide ligase), 42 (deoxycytidylate hydroxymethylase), 43 (DNA polymerase), rIIA, rIIB, and e (endolysin). The principal results are: (I) All of the genes studied were transcribed exlusively from the so-called l-strand of phage DNA. (2) DNA synthesis and the maturation-defective proteins were required to turn-off transcription of genes 42, rIIA, tIIB, and 43. Experiments performed with chloramphenicol suggested that all phage-specific proteins required to turn-off transcription of these genes were not present until 6 to 8 min post infection (p.i.). (3) During a normal developmental programme, gene 30 was transcribed throughout the eclipse. DNA-negative and maturation-defective conditions had no obvious effect on transcription of this gene. (4) During a normal lytic event, two discrete waves of gene e transcription were observed. The late wave was dependent upon DNA-synthesis and presence of functional maturation-defective proteins. The early wave was unaffected by DNA-negative or maturation-defective conditions. Experiments with chloramphenicol indicated that, if any virus-specific proteins are involved with regulation of early e transcription, such proteins are present by 3 min p.i. The data are interpreted to mean that early gene transcription is regulated by a minimum of two mechanisms. One of these mechanisms is fully operational by the 3rd min and, among the genes studied, controlled early e transcription. A second mechanism becomes operational between 6 and 8 min p.i. and controls transcription of genes 42, 43, rIIA, and rIIB.

Animals↗
PubMed1976

Correlation of structural transitions in coliphage R17 with its loss of infectivity.

A circular dichroism comparative study of isolated and in situ phage R17 RNA reveals in both cases the same degree of base pairing. However, thermal circular dichroism melting profiles exhibit the presence of free energy of interaction between RNA and capsid protein. It is apparent that the capsid stabilizes the RNA structure with and without the addition of Mg2+. A close RNA capsid association is also derived from pH titration circular dichroism studies. The pH melting of the RNA in situ starts to occur about 0-5 pH unit higher with and without the addition of Mg2+ than the acid denaturation of isolated RNA. A direct correlation between bathochromic CD peak shift to the main position band and loss of survivors is noted for the thermal melting as well as pH titration experiments. It is suggested that the heat and pH induced conformational alterations of R17 RNA in situ coinciding with loss of infectivity occur after an in situ alteration of nucleic acid-capsid protein interaction.

Capsid↗
PubMed1983

Genetic studies of hybrids between coliphage phi 80 and Salmonella phage P22.

Hybrids between Escherichia coli phage phi 80 and Salmonella typhimurium phage P22 were isolated after superinfection by P22 of a smooth E. coli-S. typhimurium hybrid lysogenic for phi 80. These hybrid phages, designated phi 80immP22 and phi 80immP22dis, possessed the phi 80 protein coat and tail genes. The phi 80immP22 hybrids acquired the immunity (immC) region of P22 and some adjacent P22 genes, but E. coli-S. typhimurium strains lysogenic for phi 80immP22 hybrids remained sensitive to P22. The phi 80immP22dis hybrids, found ten times more frequently than the phi 80immP22 hybrids, contained a more extensive portion of the P22 genome which encompassed the immI as well as the immC region of P22. Therefore, the phi 80immP22dis hybrids conferred on their hosts immunity to P22 infection. Further analyses have revealed that the phi 80immP22dis hybrids carry the P22 attachment region and either P22 tail gene 9 or antigen conversion gene a1, but not both of these genes.

Coliphages↗
PubMed1985

High frequency transduction by phage hybrids between coliphage phi 80 and Salmonella phage P22.

phi 80immP22dis, a hybrid between phi 80 and P22, carries all the late genes of phi 80 and most of the P22 early region including the immC and immI bipartite immunity loci. The presence of the immI region allows this hybrid to grow on lysogens of phi 80immP22 hybrids which have the immC locus, but not the immI locus. In addition to these P22 immunity regions, phi 80immP22dis contains the P22 att marker so that the prophage can be inserted into the chromosomal P22 attachment site adjacent to the proA-proB region of the host. Unlike its phi 80 parent which performs specialized transduction of the trp region, phi 80immP22dis transduces markers located adjacent to its attachment site to Escherichia coli K12 recipients at high frequencies (0.3% for argF and 0.18% for proA). Induction of phi 80immP22dis lysogens yields new hybrid phage clones which have incorporated E. coli K12 chromosomal segments in place of the P22 immI to att segment. Having lost the immI region, the new hybrids no longer grow in phi 80immP22 lysogens. These new hybrids, termed phi 80immP22dis-, possess specialized transducing properties, transferring the argF and proA markers at higher frequencies (21% for argF and 12% for proA) than previously obtained with the phi 80immP22dis phage.

Coliphages↗
PubMed1986

Two groups of capsule-specific coliphages coding for RNA polymerases with new promoter specificities.

Four bacteriophages (A16, CK235, phi 1.2 and K31) which specifically attack different encapsulated strains of Escherichia coli have been shown to be related to bacteriophage T7 (which is unable to grow on encapsulated hosts). The conclusion that phages A16 and CK235 are related to T7 is based on similarities in the pattern of expression of intracellular phage proteins, early appearance, in infected host cells, of a phage DNA-specific RNA polymerase and hybridization (albeit to a low extent) of A16 DNA and of CK235 DNA to T7 DNA. The first two criteria also apply to phages phi 1.2 and K31 but hybridization of their DNAs with T7 DNA could not be detected. The RNA polymerases of CK235 and A16 have similar template specificities and the same applies to the RNA polymerases of phi 1.2 and K31. None of the new RNA polymerases can use T7 DNA as template.

Coliphages↗
PubMed1978

Transduction of Myxococcus virescens by coliphage P1CM: generation of plasmids containing both phage and Myxococcus genes.

Chloramphenicol-resistant Myxococcus virescens were obtained by infecting myxococci with Escherichia coli specialized transducing phage P1CM. The drug-resistant myxococci were phenotypically unstable. They contained more than one type of plasmid; these plasmids were not found in the parent strain. Chloramphenicol-resistant E. coli were obtained by transformation with either a fraction of myxococcal DNA containing the plasmids or with P1CM prophage DNA. These transformants contained plasmids. Escherichia coli transformed by DNA from the myxococci contained both P1CM and myxococcal genes. Individual transformant clones differed in the genetic make-up of their plasmids. Among the myxococcal genes expressed in these plasmid-harbouring E. coli strains were a capacity for self-transmissibility and a pattern of phage sensitivity characteristic of R factor incompatibility group W. Escherichia coli transformed with P1CM prophage contained incomplete P1CM genomes; none of the chloramphenicol-resistant transformants produced P1CM phage particles. The significance of these findings for an understanding of mechanisms for the generation of R factors is discussed.

Chloramphenicol↗
PubMed1981

Characterization of bacteriophage j2 of Salmonella typhi as a generalized transducing phage closely related to coliphage P1.

Phage j2, a lysogenic phage in Salmonella typhi J2, was shown to produce tiny plaques on various Vi type strains of S. typhi, to be a generalized transducing phage, and to have many characteristics including a serological one in common with phage P1 of Escherichia coli. Lysogenization of various S. typhi type strains with j2 or P1-group phages usually resulted in the alteration of the phage types of the S. typhi strains, except that phage j2 did not cause alteration of type 53. Phage j2 transduced, at high frequencies, much larger DNA molecules (up to at least 70 megadaltons) than those known to be transduced by Salmonella phage P22: this should prove useful for the genetic analysis of S. typhi.

Adsorption↗
PubMed1987

Co-adaptation of Escherichia coli and coliphage lambda vir in continuous culture.

Populations of the bacterium Escherichia coli and of its phage lambda vir appeared to equilibrate in continuous cultures. The bacterial end-populations were heterogeneous in respect of their resistance to lambda vir and their ability to utilize maltose. The most competitive of the selected bacteria were mutants which had a reduced rate of synthesis of lambda-receptor so as to become highly, but not totally, resistant to the phage. The coexisting phage had an increased affinity for the receptor and an altered antigenic specificity, suggesting adaptation of its adsorption site in response to the evolution of resistance in the bacteria.

Adaptation, Physiological↗
PubMed1976

Temperate coliphage HK022. Clear plaque mutants and preliminary vegetative map.

Wild type phage HK022 was mutagenized by N-methyl-N'-nitro-N-nitrosoguanidine to induce clear plaque mutants. A total of 225 clear plaque mutants were isolated and 198 of these were assignable to one or the other of two complementation groups of the corresponding cistrons which have been designated as cI and cII, respectively. Approximately 25% of the c mutants were found to be temperature-sensitive (cts); producing turbid plaques at 32 C and clear plaques at 38 C and above. From complementation tests involving cI and cII mutants, bacteria lysogenic for cII prophage were frequently obtained. Double lysogens harboring a CI and a cII prophage were infrequently found and single lysogens harboring only a cI prophage have not been recovered. Bacterial lysogens harboring a prophage carrying a cts mutation in the cI cistron were readily obtainable. However, such lysogens show a lethal phenotype at 40 C and above, although they appear to be fully viable at 32 C. It is shown that by incubation of lysogens harboring a cts mutant of the cI cistron at 42 C, it is possible to isolate cryptic lysogens which are non-immune but harbor at least one of the phage sus+ alleles. Genetic data involving cI, cII, and two complementing sus mutants of essential genes are presented. From these data the following vegetative map is deduced: sus4--cII-cI-sus3.

Coliphages↗