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PubMed1996

The Mu strong gyrase-binding site promotes efficient synapsis of the prophage termini.

A strong DNA gyrase-binding site (SGS) is located midway between the termini of the bacteriophage Mu genome and is required for efficient replicative transposition. We have proposed that the SGS promotes the efficient synapsis of the Mu prophage ends (an obligate early step in replicative transposition), and that it does so by helping to organize the prophage DNA into a supercoiled loop with the SGS at the apex of the loop and the prophage termini at the base. The positioning of the synapsing termini equidistant from the SGS is a key element in the proposed model. To test this proposal, we have constructed prophages with a second, internal right end and asked whether the natural, external right end or the internal right end is used for synapsis with the left end in the presence and absence of the SGS. In the presence of the central SGS, the natural, or outside, right end was used exclusively and very efficiently. In the absence of the central SGS, the internal right end was used preferentially and inefficiently: the efficiency of transposition decreased with increasing distance between the internal right end and the left end. Repositioning the SGS midway between the left end and an internal right end allowed highly efficient use of the internal right end. These results support a model in which gyrase can influence long-range DNA interactions to promote efficient synapsis of Mu prophage ends.

Bacteriolysis↗

PubMed1999

Inducible prophages contribute to Salmonella virulence in mice.

We show that Salmonella typhimurium harbours two fully functional prophages, Gifsy-1 and Gifsy-2, that can be induced by standard treatments or, more effectively, by exposing bacteria to hydrogen peroxide. Curing bacteria for the Gifsy-2 prophage significantly reduces Salmonella's ability to establish a systemic infection in mice. Cured strains recover their virulence properties upon relysogenization. Phage Gifsy-2 carries the sodC gene for a periplasmic [Cu,Zn]-superoxide dismutase previously implicated in the bacterial defences against killing by macrophages. The contribution of the Gifsy-1 prophage to virulence - undetectable in the presence of Gifsy-2 as prophage - becomes significant in cells that lack Gifsy-2 but carry the sodC gene integrated in the chromosome. This confirms the involvement of Gifsy-2-encoded SodC protein in Salmonella pathogenicity and suggests that the Gifsy-1 prophage carries one or more additional virulence genes that have a functional equivalent on the Gifsy-2 genome.

Animals↗

PubMed1970

Split-operon control of a prophage gene.

Both prophage integration in bacteriophage P2 and the reverse event, prophage excision, are known to require a specific phage gene product, the so-called int function. We find that P2 can integrate efficiently at a free attachment site also in an immune host (i.e., in the presence of phage specific repressor) provided the superinfecting phage is not deficient in int function. Prophage P2, on the other hand, is not excised from the host chromosome even in a derepressed lysogen unless int function is supplied by a superinfecting phage. Thus, the int function of P2 is expressed constitutively by the superinfecting phage, but is not expressed by the prophage even in the absence of phage repressor. It is proposed that the int function of P2 is not controlled by phage repressor, but belongs instead to a constitutive operon that is physically disrupted by prophage integration.

Cell Transformation, Neoplastic↗

PubMed1971

On the process of cellular division in Escherichia coli: replication of the bacterial chromosome under control of prophage P2.

The temperature-sensitive mutant CRT46 of Escherichia coli K12 is unable to initiate new rounds of DNA replication at 42 degrees C. Mutants of bacteriophage P2 have been isolated, which, in the prophage state, allow mutant CRT46 to grow at 42 degrees C. The lysogenic bacteria that grow at 42 degrees C are apparently replicating under the control of prophage P2, which substitutes for the bacterial initiation system. The ability of prophage P2 cause this suppression phenomenon depends on the position of the prophage on the bacterial chromosome. Those lysogenic strains that are able to grow at 42 degrees C all carry the prophage close to metE. The P2 mutants that allow CRT46 to grow at 42 degrees C have insertions in the early region of the P2 genome. The suppression requires the cis-acting protein formed by gene A of P2.

Cell Division↗

PubMed1983

The induction of prophage expression in different Salmonella typhimurium strains by DNA cross-linking and monoadduct forming psoralens and longwave ultraviolet radiation.

The cytotoxicity, and ability to induce the expression of prophage in Salmonella typhimurium LT2 strains has been examined for 4 furocoumarins, 8-methoxypsoralen (8-MOP), 5-methoxypsoralen (5-MOP), 3-carbethoxypsoralen (3-CP), and 5-methylisopsoralen (5-MI) given with ultraviolet-A radiation (u.v.A). 8-MOP and 5-MOP have a linear tricyclic structure and possess two photoreactive sites, the 3,4 and 4',5' double bonds, enabling them to form both monoadducts and interstrand cross-links with DNA. The angular structure of 5-MI imposes steric constraints preventing it from forming interstrand cross-links with DNA although it possesses both of the photoreactive double bonds. The substituent group at position C-3 in 3-CP blocks the 3,4 reactive site and 3-CP is thus incapable of forming interstrand cross-links; 3-CP is reportedly, unlike the other three furocoumarins, non-carcinogenic in mice. 8-MOP, 5-MOP, and 5-MI were very cytotoxic to both the base-pair (TA1535) and frame-shift (TA1538) tester strains when given with u.v.A. Comparable amounts of 3-CP given with u.v.A were much less toxic. 8-MOP, 5-MOP, and 5-MI were potent inducers of prophage expression in both TA1535 and TA1538. 3-CP was a very poor inducer of prophage. The cytotoxicity and prophage inducing ability of 5-MI + u.v.A indicate that these actions are not necessarily restricted to the DNA crosslinking psoralens. The lower toxicity of 3-CP + u.v.A is not a simple function of the ability of 3-CP to form only monoadducts with DNA. The ability or inability to induce the expression of prophage in S. typhimurium may be a rapid and useful screen for the potential phototoxicity and carcinogenicity of novel psoralens.

DNA, Bacterial↗

PubMed1980

Selection of Bacillus subtilis 168 mutants with deletions of the PBSX prophage.

Heat-resistant derivatives of a Bacillus subtilis 168 strain carrying an xhi mutation, which causes heat-sensitive induction of the PBSX prophage, have been isolated and screened for the acquisition of auxotrophy. Two classes of auxotrophs were isolated, namely Pro- and Pro-Met-; they lacked the ability to produce PBSX, as shown by their resistance to mitomycin C-induced lysis. The proline and methionine requirements and the resistance to mitomycin C were shown to segregate together in phage PBS1-mediated transduction crosses and to be linked to thiB, which is known to be co-transducible with the PBSX prophage. It was therefore proposed that these strains had deletions which removed all or part of the PBSX prophage together with adjacent bacterial DNA encoding the pro(AB) and metC genes. The met mutation was shown to be metC in PBS1 transduction crosses; this gene is known to be co-transducible with the PBSX prophage. The proline requirement was probably due to the deletion of a pro gene which was demonstrated to lie between the PBSX prophage and metC and which was 90% co-transducible with metC. These deletions have been transduced into a strain which was cured of phage SP beta, another bacteriophage carried by B. subtilis 168. No phage particles could be seen in mitomycin C-induced cultures of such strains. The PBSX-deletion strains grew with the same generation time as the PBSX+ parent in L-broth (27 min at 35 degrees C) but they were slower in minimal medium (e.g. 72 min as against 51 min in the PBSX+ strain). Besides being resistant to mitomycin C-induced lysis, the deletion strains were also resistant to lysis induced by thymine starvation of thymine auxotrophs and the loss of viability of these strains after thymine starvation was 100-fold less than in the PBSX+ parent. The deletion strains had not, however, lost the bacterial autolytic enzymes, since they were still susceptible to lysis when placed under semi-anaerobic conditions.

Bacillus subtilis↗

PubMed2000

Diversity in the arrangement of the CTX prophages in classical strains of Vibrio cholerae O1.

This study reports the results of a molecular analysis of the CTX prophages in classical biotype strains of Vibrio cholerae O1 of clinical origin isolated between 1970 and 1979 in India. All strains were sensitive to group IV classical phage and polymyxin B but resistant to group 5 El Tor phage. These phenotypic traits are consistent to that exhibited by the classical biotype. PCR studies reconfirmed their biotype assignment and showed the presence of intact CTX prophages and the presence of the recently described toxin linked cryptic plasmid. Restriction fragment length polymorphism of rRNA genes and pulsed-field gel electrophoresis showed clonal diversity among the strains. The most notable observation was the finding that one strain (GP13) has three CTX prophages while another (GP147) has four CTX prophages. This is the first time heterogeneity is reported in the arrangement of the CTX prophages among classical strains of V. cholerae O1.

Bacteriophage Typing↗

PubMed1987

Bacteriophage Resistance Plasmid pTR2030 Inhibits Lytic Infection of r(1)t Temperate Bacteriophage but Not Induction of r(1)t Prophage in Streptococcus cremoris R1.

The effects of pTR2030 on the replication of four small isometric bacteriophages were examined in Streptococcus cremoris R1. Three lytic phages (652, 720, and 751), which were isolated independently over a 29-year period, were unable to form plaques on a pTR2030 transconjugant of S. cremoris R1. The fourth phage evaluated, phage r(1)t, was a temperate phage induced from S. cremoris R1 by treatment with mitomycin C. A prophage-cured derivative of S. cremoris R1, designated R1Cs, was isolated and served as a lytic indicator for phage r(1)t. Strain R1Cs and a derivative of this strain that was relysogenized with r(1)t, designated R1Cs(r(1)t), were used as conjugal recipients for transfer of the phage resistance plasmid pTR2030. pTR2030 transconjugants of strains R1Cs and R1Cs(r(1)t) were evaluated for sensitivity to r(1)t phage and induction of r(1)t prophage, respectively. The temperate phage r(1)t adsorbed eficiently but did not form plaques on the prophage-cured, pTR2030 transconjugant strain T-R1Cs. However, in the r(1)t lysogen [T-R1Cs(r(1)t)], pTR2030 did not inhibit prophage induction with mitomycin C, cell lysis, or production of infective r(1)t phage particles. The data demonstrated that pTR2030-induced resistance inhibited lytic infection by r(1)t phage from without but did not retard lytic development after prophage induction within the cell. It was suggested that pTR2030-encoded phage resistance to small isometric phages may, therefore, act at the cell surface or membrane to prevent phage DNA passage into the host cell or inhibit early events required for lytic replication of externally infecting phage.

Journal Article↗

PubMed1973

Effect of the prophage and penicillinase plasmid of the recipient strain upon the transduction and the stability of methicillin resistance in Staphylococcus aureus.

Transduction of a methicillin-resistance determinant (mec) in Staphylococcus aureus RN450 was dependent on its prior lysogenization with an appropriate temperate phage. In addition, an appropriate transduced penicillinase plasmid was usually required. Some phage 80-resistant variants of RN450 or of its parental lysogenic strain, NCTC 8325, were also effective recipients for transduction of mec. Elimination of prophage from RN450 abrogated its effectiveness as a transductional recipient of mec. Elimination of prophage from a methicillin-resistant transductant of RN450 reduced resistance to undetectable levels in six of seven phage-eliminated strains. In four of these a variable number of clones again became phenotypically resistant after lysogenization alone or lysogenization combined with reintroduction of a penicillinase plasmid. In two prophage-eliminated strains, no evidence of residual mec could be adduced. The establishment, expression, or stability of the transduced mec in strain RN450 appeared to depend on some function determined by a prophage or a prophage and a penicillinase plasmid.

Chromosomes, Bacterial↗

PubMed1975

Prophage-dependent plasmid integration in Staphylococcus aureus.

A study has been done of reversion to thermostability of thermosensitive, replication-defective (TSR) mutant penicillinase plasmids. All three of the expected classes of reversions were encountered: back mutation, suppression, and integration. The latter class was examined in some detail and it was found that the presence of the phi 11 phophage enhance the frequency of reversion by integration some 103-fold. Prophage-dependent integration resulted in inactivation of plasmid-linked arsenate and arsenite resistance; these revertant strains gave rise to high frequency tranducing lysates where the plasmid was restored upon transduction to its original TSR state including recovery of these resistances. The integrated plasmid-prophage complexes were stable at high temperatures (43 C) but slow growing and unstable at low (32 C); loss of either plasmid or prophage restored normal growth and stability. Sometimes restoration of the plasmid to its autonomous TSR state was observed and molecular studies showed that in most cases the plasmid was essentially the same size as before integration. In some cases an excision complex was recovered that was more than twice the size of the plasmid and could have been a plasmid-phage co-integrate. Integration also took place in the absence of the ł 11 prophage. These integrations retained all plasmid-linked resistances, were stable at all temperatures, and gave rise to low frequency transducing lysates in which the integrated state was retained upon transduction. On the basis of these results it is suggested that the prophage promotes integration at or near its attachment site.

Arsenates↗

PubMed1990

Integration of bacteriophage lambda into the cryptic lambdoid prophages of Escherichia coli.

Bacteriophage lambda missing its chromosomal attachment site will integrate into recA+ Escherichia coli K-12 and C at the sites of cryptic prophages. The specific regions in which these recombination events occur were identified in both lambda and the bacterial chromosomes. A NotI restriction site on the prophage allowed its physical mapping. This allowed us to identify the locations of Rac, Qin, and Qsr' cryptic prophages on the NotI map of E. coli K-12 and, by analogy, to identify the cryptic prophage in E. coli C as Qin. No new cryptic prophages were detected in E. coli K-12.

Bacteriophage lambda↗

PubMed1986

Evidence for circular permutation of the prophage genome of Bacillus subtilis bacteriophage phi 105.

Analysis of DNA extracted from Bacillus subtilis lysogenic for bacteriophage phi 105 was performed by restriction endonuclease digestion and Southern hybridization using mature phi 105 DNA as a probe. The data revealed that the phi 105 prophage is circularly permuted. Digests using the enzymes EcoRI, SmaI, PstI, and HindIII localized the bacteriophage attachment site (att) to a region 63.4 to 65.7% from the left end of the mature bacteriophage genome. The phi 105 att site-containing SmaI C, PstI J, and HindIII L fragments were not present in digests of phi 105 prophage DNA. phi 105-homologous "junction" fragments were visualized by probing digests of prophage DNA with the purified PstI J fragment isolated from the mature bacteriophage genome. The excision of the phi 105 prophage was detected by observing the appearance of the mature PstI J fragment and the concomitant disappearance of a junction fragment during the course of prophage induction.

Bacillus subtilis↗

PubMed1985

[Mutagenic effect of o-methylhydroxylamine on the prophage and extracellular phage lambda].

Induction of c-mutations in extracellular bacteriophage and prophage lambda cI857 ind-treated with 1 M O-methylhydroxylamine (OMHA) at 32 degrees and pH 5.6 has been studied. The frequency of c-mutations increases proportionally to the time of treatment of extracellular phage and does not depend on cellular recA+ or polA+ functions and on induction of SOS-repair system caused by UV-irradiation of host cells. Prophage is inactivated and mutagenized approximately 10-fold faster than extracellular phage immediately after treatment of lysogenic cells during prophage induction. Thus, prophage survival does not depend on repair functions of the host cells, and the frequency of c-mutations in recA and, especially, in polA lysogens is significantly lower, than in the wild-type cells. Delayed thermoinduction (90 min) of prophage causes significant enhancement of survival and decreases the frequency of c-mutations in all strains studied. Preliminary treatment of non-lysogens with OMHA does not increase the frequency of c-mutations in undamaged phage or in phage treated with OMHA in vitro.

Bacteriophage lambda↗

PubMed1988

[Localization of prophage SM of Pseudomonas aeruginosa in the chromosome of host cells].

Pseudomonas aeruginosa PAO SM-prophage was localized on the chromosome between thr-9001 and pur-66 locuses on 42-43 min of chromosomal genetic map. The location of prophage was identified on the basis of prophage linkage with the above-mentioned markers and confirmed by the purine, hypoxanthine and threonine deletions in course of thermoinduction of SM cts6 prophage from lysogens. The decrease for two orders in lysogenization frequency of thr mutants by SM bacteriophage suggests the integration of SM prophage in these cells into some other region of chromosome.

Bacteriophages↗

PubMed1983

Mutagenic response of Ames strains cured of their inducible Fels 1 and Fels 2 prophages.

Ames strain TA100 was cured of its Fels 1 and Fels 2 prophages to yield the corresponding nonlysogenic derivative designated TAQ100. The two monolysogenic strains corresponding to TA100 lysogenic for Fels 1 (TAQ100F1) and for Fels 2 (TAQ100F2) were also isolated. In addition, the equivalent strains lacking pKM101 and designated TAQ1535, TAQ1535F1, and TAQ1535F2 were obtained. Ames strains TA98 and TA1538 are lysogenic for Fels 2 and were observed by colony hybridization to contain cryptic Fels 1 DNA sequences. Strains corresponding to TA98 and TA1538 cured of Fels 2 were isolated and designated TAQ98F1d and TAQ1538F1d, respectively. Fels 1 grew poorly on Fels 1-cured strains, and Fels 2 grew not at all on Fels 2-cured strains. The cured strains had therefore to be identified as such by their failure to react in colony hybridization with 32P-labeled probes of Fels 1 and/or Fels 2 DNA. The specificity of the labeled probes was confirmed with the aid of the nonlysogenic Salmonella typhimurium strain Q1 and its two monolysogenic derivatives Q1 (Fels 1) and Q1 (Fels 2). The cured strains were found to respond in the same manner as did the standard Ames strains to a variety of well-known mutagens, including aflatoxin B1, 7, 12-dimethylbenz(a)anthracene, daunorubicin, 2-amino-dipyrido[1,2-a:3',2'-d]imidazole, and beta-naphthylamine. Also, mitomycin C, bleomycin, and diethylstilbestrol were nonmutagenic to TAQ100 and TAQ98F1d as they are to TA100 and TA98. Since the Fels prophages are inducible by aflatoxin B1, by daunorubicin, and by other agents, it seems that mutagenesis and Fels prophage induction occur in separate subpopulations of cells; this situation had previously been reported to occur for mutagenesis and prophage lambda induction in Escherichia coli. In any case, the Fels prophages appear to have no major influence on the mutagenic response of the Ames strains.

Antineoplastic Agents↗

PubMed2025

Diverse defense systems and prophages in human-associated Bifidobacterium species reveal coevolutionary "arms race" dynamics.

Bacteria of the genus Bifidobacterium are pivotal for human health, especially in early life, where they dominate the gut microbiome in healthy infants. Bacteriophages, as drivers of gut bacterial composition, can affect bifidobacterial abundance. Here, we use a bioinformatics approach to explore direct interactions between human-associated Bifidobacterium spp. and prophages, as evidenced by their genomes. Analysis of 1,086 bifidobacterial genomes reveals the presence of complex systems that prevent viral invasion, with 34 defense systems and 56 subtypes detected, including several different CRISPR-Cas systems. CRISPR spacers target almost three-quarters of bifidobacteria-derived prophages, indicating dynamic interactions. At least one prophage is present in ∼67% of strains, with phages exhibiting high genomic diversity and evidence of historical recombination. These prophages encode various defense and anti-defense systems, such as anti-CRISPR genes and restriction-modification mechanisms. Overall, this investigation reveals that coevolutionary "arms race" dynamics drive genomic diversity in both bifidobacteria and their phages.

Prophages↗

PubMed2026

Prophage Activation as an Overlooked Mechanism Underlying the Biocidal Effect of Free Nitrous Acid in Sewers.

Biogenic hydrogen sulfide produced in sewer systems causes odor nuisance and concrete corrosion, necessitating effective biocidal control. Free nitrous acid (FNA) has emerged as a promising biocide, but its unclear mechanisms complicate dosage optimization and risk assessment. Here, using Desulfovibrio vulgaris as a model lysogenic bacterium, we demonstrate that low-dose FNA (0.2-4.0 mg N/L) induces bacterial inactivation via prophage activation-associated lysis in addition to chemical oxidation. Reactive nitrogen species (RNS) scavenging tests revealed that RNS-mediated oxidative stress was closely associated with prophage activation. Activated phages further infected new hosts, reducing the viability of freshly cultured D. vulgaris cells by 25.7% and increasing total phage production 15.2-fold. The phenomenon was further validated in real sewage biofilms, where increased phage production and decreased bacterial viability were observed at a low FNA dose of 0.2 mg N/L, below the dose required for cell destruction by chemical oxidation. Furthermore, metagenomic analysis of 896 sewage samples worldwide revealed that 71.9% of recovered sewage-derived microbial genomes harbor prophages, indicating a widespread genomic basis for prophage activation-mediated bacterial inactivation. Overall, this study expands current understanding of the biocidal mechanisms of FNA and contributes to the development of environmentally sustainable biocidal strategies.

Nitrous Acid↗

PubMed2006

Spontaneous recombination between homologous prophage regions causes large-scale inversions within the Escherichia coli O157:H7 chromosome.

It is known that XbaI-digested chromosomal DNAs of strains of Escherichia coli O157:H7 exhibit a wide variety in pulsed-field gel electrophoresis (PFGE) fragment patterns, which is used for epidemiological surveillance of this important pathogen. The variety in the restriction enzyme-digestion patterns suggests a wide genomic diversity, however, only a few studies have been conducted to investigate involvement of large-scale chromosomal rearrangements in development of the diversity. In this study, through rounds of subculturing E. coli O157:H7 strain EDL933, naturally occurring genome variation in the isolated derivatives was investigated. By comparing the PFGE patterns among clonally related derivatives, we found five types of large-scale inversions taking place within the chromosome. The five inversions found were across the replication axis and ranged from 250-kb to 1.4-Mb long, and all the corresponding recombination sites were associated with prophages or phage-like regions. Four inversions out of the five were resulted from recombination between pairs of lambda-like prophages disturbing the symmetry of the origin and terminus of the replication axis. These observations indicate that those prophage regions represent some of the hot spots for intrachromosomal recombination within the E. coli O157:H7 chromosome, where recombination between the prophage regions results not only in the large chromosomal inversions but might also in generation of chimeric phages.

Cells, Cultured↗