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PubMed2005

Demonstration of cotranscription and 1-methyl-3-nitroso-nitroguanidine induction of a 30-gene operon of Borrelia burgdorferi: evidence that the 32-kilobase circular plasmids are prophages.

The Borrelia genome is comprised of linear and circular elements, including a group of 32-kb circular plasmids (cp32s). Earlier analyses identified a bacteriophage, varphiBB-1, that may package cp32s, suggesting that these plasmids are prophages. cp32-8, cp32-9, and cp32-1 (plasmids L, N, and P, respectively) encode virulence factors such as the factor H binding, OspE proteins (BBL39, BBN38, and BBP38). Here the expression patterns of cp32-8 open reading frames (ORFs) in in vitro-cultivated 1-methyl-3-nitroso-nitroguanidine (MNNG)-treated and untreated spirochetes and during infection were assessed. ORFs BBL42 through BBL28, which encode several bacteriophage protein homologs, were found to be cotranscribed and expression was upregulated by MNNG. Immunoblotting revealed that MNNG-induced transcription led to increased protein production. The expression of several genes that reside outside of the BBL42-BBL28 operon was not affected by MNNG. Some of these genes, including OspE (BBL39), appear to represent morons. Real-time reverse transcription-PCR of spirochetes in mouse tissue revealed that although the phage operon was not induced during infection, transcription of BBL23 (previously designated BlyA), a putative holin, was upregulated. This observation indicates that some genes within the operon can be independently transcribed from internal promoters. Additional transcriptional analyses of the operon identified multiple transcriptional start sites and provided evidence for the expression of a homologous operon from other cp32s. The data support the hypothesis put forth by C. Eggers and D. S. Samuels (J. Bacteriol. 181:7308-7313, 1999) that the cp32s are prophages, a finding with broad implications for our understanding of Borrelia pathogenesis and Borrelia genome evolution.

Animals↗

PubMed1999

Prophage carriage as a molecular epidemiological marker in Streptococcus pneumoniae.

The great majority of clinical isolates of Streptococcus pneumoniae carry prophages that may be identified through their hybridization with a DNA probe specific for the pneumococcal lytA gene (M. Ramirez, E. Severina, and A. Tomasz, J. Bacteriol. 181:3618-3625, 1999). We now show that the lytA hybridization pattern of chromosomal SmaI digests is stable for a given strain during extensive serial culturing in the laboratory; the pattern is specific for the strain's clonal type, as defined by pulsed-field gel electrophoretis (PFGE) pattern, and variations in PFGE subtypes may be explained by changes in the number and chromosomal localization of this prophage(s). These observations indicate that the lytA hybridization pattern may be used as a molecular epidemiological marker that offers additional resolution of the genetic background of S. pneumoniae strains.

Bacteriophages↗

PubMed1973

Heat induction of prophage phi 105 in Bacillus subtilis: bacteriophage-induced bidirectional replication of the bacterial chromosome.

A mutant of Bacillus subtilis, dna-1, which cannot initiate new rounds of DNA replication (obtained from N. Sueoka) was lysogenized with wild-type phi 105 and with the heat-inducible mutant phi 105 cts23. Bacteria were incubated at the permissive temperature in the presence of chloramphenicol and then shifted to the nonpermissive temperature where induction of phi 105 cts23 occurs. DNA made after the shift was labeled with a density label, and the distribution of bacterial and phage markers in replicated and unreplicated DNA was determined. Similar experiments were performed with nonlysogenic dna-1 infected with phage phi 105 cts23 after the temperature shift. The results show that after induction of phi 105 cts23 prophage, bacterial markers on either side of the prophage replicate at an increased rate compared to more distant markers. No selective stimulation of bacterial DNA synthesis was observed on infection or after shifting bacteria lysogenic for noninducible phage to the higher temperature. Attempts to suppress the initiation mutation dna-1 by phage phi 105 were unsuccessful.

Bacillus subtilis↗

PubMed1974

Prophage induction of noninducible coliphage 186.

Coliphage 186 has been regarded as a member of the noninducible group of coliphages. Evidence that prophage 186 is induced by ultraviolet irradiation or by treatment with nalidixic acid or mitomycin C is now presented. The phage yields were similar to those from lysogens of the inducible phage lambda, and the induction required a recA(+) host. A noninducible mutant of 186 was isolated from its heat-inducible derivative, 186cIts, that was no longer inducible by ultraviolet irradiation but remained heat inducible. That zygotic induction of 186 after transfer from a lysogenic male to a non-lysogenic recipient did not occur is indicated by the following findings: (i) there was only a slight increase in phage titer; (ii) similar levels of recombinants were obtained for markers adjacent or distal to the phage integration site, whether the recipient was lysogenic or not, and there was no effect on the gradient of marker transfer; (iii) lysogenic recombinants were readily found and the co-transfer of 186 with adjacent markers was the same to lysogenic or non-lysogenic recipients. Thus, 186 formed an inducible prophage that did not display zygotic induction. Nevertheless, it shared many properties with the noninducible phage P2 as outlined in the discussion.

Coliphages↗

PubMed1975

Isolation and characterization of prophage mutants of the defective Bacillus subtilis bacteriophage PBSX.

Bacillus subtilis mutants with lesions in PBSX prophage genes have been isolated. One of these appears to be a regulatory mutant and is defective for mitomycin C-induced derepression of PBSX; the others are defective for phage capsid formation. All of the PBSX structural proteins are synthesized during induction of the capsid defective mutants; however, several of these proteins exhibit abnormal serological reactivity with anti-PBSX antiserum. The two head proteins X4 and X7 are not immunoprecipitable in a mutant which fails to assemble phage head structures. In the tail mutant, proteins X5 and X6 are not immunoprecipitable, tails are not assembled, and a possible tail protein precursor remains uncleaved. The noninducible mutant does not synthesize any PBSX structural proteins after exposure to mitomycin C. The mutation is specific for PBSX since ø105 and SPO2 lysogens of the mutant are inducible. All of the known PBSX-specific mutations were shown to be clustered between argC and metC on the host chromosome. In addition, the metC marker was shown to be present in multiple copies in cells induced for PBSX replication. This suggests that the derepressed prophage replicates while still integrated and that replication extends into the adjacent regions of the host chromosome.

Antigen-Antibody Complex↗

PubMed1976

Orientation of the tox gene in the prophage of corynebacteriophage beta.

The orientation of the gene for diphtheria toxin, tox, in the prophage of converting corynebacteriophage beta has been determined. The orientation of tox in prophage and that reported simultaneously by Holmes (1976) for vegetative phage are compatible with the hypothesis that beta phage is inserted into the chromosome of its bacterial host by means of a mechanism similar to that described for lambda phage, and that the phage attachment site lies between the tox and imm genes. The position of three tox mutations that are phenotypically CRM- has also been determined. Relative to the tox-45 mutation, they are located more proximally to the end of the tox structural gene that corresponds to the amino terminal of diphtheria toxin.

Bacteriophages↗

PubMed1969

Defective bacteriophage PBSH in Bacillus subtilis. II. Intracellular development of the induced prophage.

Treatment of Bacillus subtilis strain 168 with mitomycin C caused induction of a defective prophage, PBSH. During induction, extensive deoxyribonucleic acid (DNA) synthesis took place. Concurrently, a change in marker frequency of the bacterial DNA was noticed. The frequency of only one marker, ade-16, the marker closest to the origin of the bacterial chromosome, was enhanced manyfold. DNA from whole phage particles transformed all bacterial markers at a frequency equal to that of DNA in the noninduced culture, except ade-16, the frequency of which was enhanced 30 to 100 times. Analysis of a double isotope experiment demonstrated that 14% of the phage DNA was derived from preinduction bacterial DNA. The other 86% of DNA in phage particles was DNA replicated after induction. Density label experiments with 5-bromodeoxyuridine showed that postinduction DNA synthesis took place preferentially at the origin region of the bacterial chromosome. Measurement of the molecular weight of DNA replicated after induction clearly showed that postinduction DNA replication is chromosomal. No evidence for prophage detachment and autonomous phage DNA replication was found. The data indicated that, after mitomycin C action, the bacterial chromosome under-went multiple reinitiation at the origin, while normal sequential DNA replication was stopped. The pool of replicated bacterial DNA was fragmented randomly. This DNA was packaged into PBSH particles which were released after cell lysis.

Bacillus subtilis↗

PubMed1985

Detection and physical map of a omega tox+-related defective prophage in Corynebacterium diphtheriae Belfanti 1030(-)tox-.

A library of chromosomal DNA from Corynebacterium diphtheriae Belfanti 1030(-)tox- was cloned in the lambda phage vector EMBL4 and screened for sequences homologous to corynephage omega tox+ and the attB1-attB2 region of the C7(-)tox- chromosome. Two portions of the 1030(-)tox- chromosome, 35 and 30.5 kilobases long which contain, respectively, the entire region homologous to corynephage omega tox+ and the attB1-attB2 sites, were mapped with the restriction endonucleases BamHI and EcoRI. Chromosomal DNA from 1030(-)tox- was shown to contain a 15.5-kilobase region that was homologous to ca. 42% of the corynephage omega tox+ genome. These sequences were found to hybridize to three regions of the phage genome and do not contain either the diphtheria tox operon or the attP site. These sequences are distant from the chromosomal region that contains the attB1-attB2 sites. Moreover, unlike other known defective prophages, the physical map of this prophage starts at the cos site and is colinear with the vegetative phage map. The 30.5-kilobase region of the 1030(-)tox- chromosome, which contains the attB1-attB2 sites, has a central core region that is almost identical to the corresponding region of the C7(-)tox- chromosome; however, the flanking sequences in these two strains of C. diphtheriae are different.

Bacteriophages↗

PubMed1970

Requirement for a functional int product in temperature inductions of prophage P22 ts mnt.

Prophage P22 ts mnt was found to be inducible by high temperatures. This property was maintained when the ts mnt allele was recombined into a phage that cannot synthesize phage deoxyribonucleic acid at high temperature. Prophage P22 int ts mnt, on the other hand, was not inducible at high temperature. This result leads to the suggestion that the int enzyme, which is involved in excision, is regulated by the product of gene mnt.

Crosses, Genetic↗

PubMed1979

The role of temperate bacteriophage SP beta in prophage-mediated interference in Bacillus subtilis.

Virulent bacteriophage phi 1 grows on a variety of Bacillus subtilis strains, mutants of this virus which abortively infect the transformable bacillus. B. subtilis 168, while retaining the ability to productively infect related bacteria have been found. In the present study, we demonstrate that the inability of one such variant, phi 1m, to develop normally in strain 168 is mediated by cryptic prophage SP beta. The latter is a temperate bacteriophage which is carried by B. subtilis 168 and most strains derived from this bacterium. Phi 1 m infection of SP beta lysogens begins with apparently normal adsorption, penetration, and inititaion of virus-directed syntheses. At about the 20th min of the latent period, however, there is an abrupt cessation of nucleic acid synthesis and cellular respiration, accompanied by a change in cell permeability. This course of events can be altered to a permissive infection by mutation in the mpi gene of SP beta, by mutation in the spoOA gene of the host, or by growing SP beta lysogens at high temperature. In addition, we found a second class of phi 1 mutants which abortively infect B. subtilis 168 derivatives even in the absence of the SP beta prophage.

Bacillus subtilis↗

PubMed2000

Effect of five dietary antimutagens on the genotoxicity of six mutagens in the microscreen prophage-induction assay.

Dietary antimutagens have been studied extensively in the last two decades, using mainly bacterial and mammalian cells. These studies have shown that certain dietary antimutagens, acting individually or as mixtures, are useful in counteracting the effects of certain mutagens and/or carcinogens to which humans are commonly exposed. However, there are some inconsistencies among publications using different bioassays. The general purpose of the research presented here was to conduct a comparative study of the antigenotoxic activity of five dietary antimutagens against six mutagens, using three rather different short-term tests: the Microscreen prophage-induction assay, the Tradescantia micronucleus test, and the Salmonella/mammalian microsome test. In this study I report the results with the Microscreen prophage-induction assay. The antimutagens selected were chlorophyllin, beta-carotene, and vitamins A, C, and E. The mutagens selected were 2-aminoanthracene, benzo[a]pyrene, 2-nitrofluorene, toxaphene, dichlorvos, and nitrofen. The results show that chlorophyllin and beta-carotene inhibited the genotoxicity of all six mutagens; vitamin E inhibited all except dichlorvos; and vitamins C and A inhibited 2-aminoanthracene, benzo[a]pyrene, 2-nitrofluorene, and nitrofen.

Antimutagenic Agents↗

PubMed1976

[Restriction and modification in Staphylococcus aureus: properties of resistance plasmids and prophages].

Experiments on elimination and transfer of resistance-plasmids in S. aureus (controlling resistance to penicillin, chloramphenicol and oxytetracycline) show that these plasmids have no restricting influence on phages used for typing of staphylococci. Prophages in lysogenic strains control a mechanism of restriction and modification which is active on phages and on chromosomal markers. The resistance-plasmids used in these experiments are insensitive to prophage controlled restriction.

Chloramphenicol↗

PubMedDate not supplied

[Prophage induction in lysogenic cultures of bacteria as a test of the biological indication of relatively low doses of gamma radiation].

Induction of prophage in lysogenic cultures, Pseudomonas aeruginosa (strain PA01 (PM63)) and Escherichia coli K-12 (strain AB1157 (lambda) pKM101), was proposed as a test for biological indication of gamma-irradiation with relatively low doses. Sufficient resolving power (the sensitivity threshold of the method was 0.25 to 0.5 Gy) and relative simplicity of the practical use of the method were demonstrated. Within the dose range from 0.25 to 10 Gy, the relationship between the value of the prophage induction and radiation dose was linear.

Bacteriophages↗

PubMedDate not supplied

[The effect of genotype on the induction of prophage lambda in E. coli cells by ionizing radiation of various LET].

A study was made of the influence of the repair genotype on lambda prophage induction by ionizing radiation of different LET in lysogenic E. coli cells. Bacterial strains W3110, P3478, GC244, and 30SO were exposed to gamma-rays and helium ions of 22 keV/microns. Induction of the prophage in GC244 and 30SO strains deficient by lexA and recA genes was either inhibited (GC244) or lacking (30SO). Inducibility of P3478 carrying polA mutation was 12 and 5 times as high as that of the wild type strain after exposure to gamma-radiation and helium ions, respectively.

Bacteriophage lambda↗

PubMed1985

[Phage-transposon interaction: the cip locus of prophage D3112 responsible for the inhibition of integration and transposition of related phage B39 of Pseudomonas aeruginosa].

Bacterial cells lysogenic for D3112, a transposable Pseudomonas aeruginosa phage restrict the growth of a related heteroimmune B39 phage. The lysogens are divided into two different types PAO(D3112). In the lysogens of the type I the efficiency of B39 growth only decreases slightly, the lysogens of the type II restricting completely the growth of this phage (e.o.p. is less than 10(-7). As shown by the results of Southern hybridization experiments, lysogens of the type I are monolysogens, while those of the type II are double or polylysogens. Restriction of B39 in PAO(D3112) is caused by expression of a locus in the D3112 genome. The locus has been termed as cip (control of interaction of phages). The cip locus was mapped at the interval 1.3-2.45 kb of the D3112 physical map using different deletion derivatives of D3112. Expression of cip only takes place in the prophage state and not during the phage lytic development. When expressed, cip affects the early steps in the growth of B39 lowering the level of integration and transposition processes; the effect is not dependent on the way of initiation of the lytic cycle (through prophage induction or infection).

Bacteriophages↗

PubMedDate not supplied

[Deletion of late genes of the prophage lambda].

The deletions in tandem prophage lambda appear with high frequency (to 10%) in rec A- strain of Escherichia coli. The deletions were shown by marker rescue and hybridization of fragments of DNA on nitrocellulose filters with nick-translated phage lambda DNA localized only in prophage area. Right and left att sites are not involved. The majority of defective lysogens had all regulatory regions and deletions of late structural genes. These strains may be used for construction of the host-vector systems with the strongest promoter p'R of phage lambda.

Bacteriophage lambda↗

PubMed1975

[Induction of prophage gamma by means of bleomycin treatment].

The kinetics of induction of lambda prophage with bleomycin A2-CP3, mitomycin C and a combination of these two antibiotics have been studied. Bleomycin has been found to cause a rapid induction of prophage in exponentially growing cultures of E. coli K12 (lambda), and the maximal values of including activity are obtained after treatment for 16 minutes with a concentration of 10 mug/ml. The per cent of induction, calculated from the total number of surviving cells, including the phage producing cells, better expresses the dynamics of the phenomenon. The number of inducing events in the population of exposed cells is proportional to the length of bleomycin treatment. These values are greater than those observed after treatment with mitomycin, at the same concentration. Inducing activity is enhanced by combination of the two antibiotics and this effect is not additive, but synergic. After the 16 minutes of treatment with bleomycin the burst sizes are lower than those which are obtained with mitomycin or with the combination of the two antibiotics. The results are interpreted as a consequence and a confirmation of the different mechanisms of action that distinguishes bleomycin from mitomycin.

Bleomycin↗

PubMed1984

Prophage induction by liver microsomal metabolites of aflatoxin B1 in lysogenic Pseudomonas aeruginosa.

Microsomal metabolites of aflatoxin B1 (AFB1) causing induction of prophage in lysogenic strain of Pseudomonas aeruginosa SM was studied. Reduction of culture turbidity was determined at various concentrations of toxin. The effect of the toxin was also studied on deoxyribonucleic acid (DNA), ribonucleic acid (RNA) and protein synthesis. AFB1 at the concentration of 50 micrograms/ml reduced initial turbidity to approximately 90% in 4 h. DNA synthesis stopped completely in the first hour but reappeared due to induction of the temperate phage. Soon after induction both RNA and protein synthesis continued but later little or no net synthesis of these macromolecules occurred. Plaque forming units (pfu) were increased approximately 90 times at 2 h as compared to the control. Testing of the effect of AFB1 on the non-lysogenic, sensitive strain demonstrated that although there was no significant decrease in culture turbidity at 50 micrograms/ml concentration of AFB1, DNA synthesis stopped completely within 1 h, while RNA and protein synthesis were increasing throughout the test interval. It has been concluded that the liver microsomal fraction of AFB1 caused induction of prophage in lysogenic cells and inhibited DNA synthesis significantly in non-lysogenic cells.

Aflatoxin B1↗