Effects of prophages HPlcl & a defective prophage carried by Haemophilus influenza Rd on transfection by phage S2 DNA.
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Bacteriophages↗
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The impact of prophages on bacterial chromosomes.
Prophages were automatically localized in sequenced bacterial genomes by a simple semantic script leading to the identification of 190 prophages in 115 investigated genomes. The distribution of prophages with respect to presence or absence in a given bacterial species, the location and orientation of the prophages on the replichore was not homogeneous. In bacterial pathogens, prophages are particularly prominent. They frequently encoded virulence genes and were major contributors to the genetic individuality of the strains. However, some commensal and free-living bacteria also showed prominent prophage contributions to the bacterial genomes. Lysogens containing multiple sequence-related prophages can experience rearrangements of the bacterial genome across prophages, leading to prophages with new gene constellations. Transfer RNA genes are the preferred chromosomal integration sites, and a number of prophages also carry tRNA genes. Prophage integration into protein coding sequences can lead to either gene disruption or new proteins. The phage repressor, immunity and lysogenic conversion genes are frequently transcribed from the prophage. The expression of the latter is sometimes integrated into control circuits linking prophages, the lysogenic bacterium and its animal host. Prophages are apparently as easily acquired as they are lost from the bacterial chromosome. Fixation of prophage genes seems to be restricted to those with functions that have been co-opted by the bacterial host.
Bacteria↗
Comparative genomics reveals close genetic relationships between phages from dairy bacteria and pathogenic Streptococci: evolutionary implications for prophage-host interactions.
The genome of the highly pathogenic M1 serotype Streptococcus pyogenes isolate SF370 contains eight prophage elements. Only prophage SF370.1 could be induced by mitomycin C treatment. Prophage SF370.3 showed a 33.5-kb-long genome that closely resembled the genome organization of the cos-site temperate Siphovirus r1t infecting the dairy bacterium Lactococcus lactis. The two-phage genomes shared between 60 and 70% nucleotide sequence identity over the DNA packaging, head and tail genes. Analysis of the SF370.3 genome revealed mutations in the replisome organizer gene that may prevent the induction of the prophage. The mutated phage replication gene was closely related to a virulence marker identified in recently emerged M3 serotype S. pyogenes strains in Japan. This observation suggests that prophage genes confer selective advantage to the lysogenic host. SF370.3 encodes a hyaluronidase and a DNase that may facilitate the spreading of S. pyogenes through tissue planes of its human host. Prophage SF370.2 showed a 43-kb-long genome that closely resembled the genome organization of pac-site temperate Siphoviridae infecting the dairy bacteria S. thermophilus and L. lactis. Over part of the structural genes, the similarity between SF370.2 and S. thermophilus phage O1205 extended to the nucleotide sequence level. SF370.2 showed two probable inactivating mutations: one in the replisome organizer gene and another in the gene encoding the portal protein. Prophage SF370.2 also encodes a hyaluronidase and in addition two very likely virulence factors: prophage-encoded toxins acting as superantigens that may contribute to the immune deregulation observed during invasive streptococcal infections. The superantigens are encoded between the phage lysin and the right attachment site of the prophage genome. The genes were nearly sequence identical with a DNA segment in S. equi, suggesting horizontal gene transfer. The trend for prophage genome inactivation was even more evident for the remaining five prophage sequences that showed massive losses of prophage DNA. In these prophage remnants only 13-0.3 kb of putative prophage DNA was detected. We discuss the genomics data from S. pyogenes strain SF370 within the framework of Darwinian coevolution of prophages and lysogenic bacteria and suggest elements of genetic cooperation and elements of an arms race in this host-parasite relationship.
Bacteriophages↗
Replication of Mu prophages lacking the central strong gyrase site.
Replication of Mu prophages lacking the central strong gyrase site (SGS) is severely slowed. To study details of the replication of these prophages, an assay was developed for determining the rate and extent of introduction of nicks at the 3'-ends of a Mu prophage, an early step in Mu replicative transposition. The maximal level of end-nicking of a prophage with the SGS, about 70-90% depending upon the host strain, was achieved within about 15 min after induction, whereas at that time less than 5% nicking was observed with a prophage lacking the SGS. The amount of nicking at the end of the SGS(-) prophage increased with time, and approx. 30% nicking of the SGS(-) prophage was achieved by 60 min post-induction. Nicking kinetics were identical at each end of the prophages, and no nicking was observed at the 5'-ends of the prophages, verifying in vivo the earlier results with in vitro systems. To determine if prophage location affects the kinetics of replication, we examined prophages at numerous chromosomal locations. SGS(+) prophages at different chromosomal locations showed essentially identical replication kinetics. SGS(-) prophages showed a range of delays in replication and host lysis. A gradient of delays was apparent, with prophages further from the chromosomal origin of replication, oriC, showing longer delays than ones nearer to oriC. However, there were also exceptions to this overall gradient. Possible explanations for the differences in the delays observed with SGS(-) prophages are discussed.
Bacteriophage mu↗
Multidimensional prophage profiling of carbapenem-resistant Enterobacteriaceae in Thailand: a nationwide, multicentre, genomic study.
BACKGROUND: Prophages influence bacterial fitness, resistance, and evolution, yet their epidemiology remains poorly understood in carbapenem-resistant Enterobacteriaceae (CRE). In this nationwide study in Thailand, we aimed to describe prophage repertoires in clinical CRE isolates and to explore their potential relevance for molecular epidemiology. METHODS: We performed a nationwide, retrospective, genomic analysis of all CRE clinical isolates collected through our previous national surveillance study involving 11 hospitals in 11 provinces in Thailand between March 25, 2012, and Jul 21, 2017. Whole-genome sequencing data from 747 CRE isolates were analysed. Intact prophages were identified using PHAge Search Tool Enhanced Release (PHASTER) and clustered by nucleotide sequence similarity. Prophage profiles were compared across multilocus sequence types, carbapenemase genotypes, specimens, geography, and patient demographics (age and sex). FINDINGS: Of the included 747 CRE isolates, 170 (23%) were Escherichia coli and 577 (77%) were Klebsiella pneumoniae. 220 (29%) of 747 strains had been isolated from female patients and 264 (35%) from male patients; metadata on patient sex were missing for 263 (35%) isolates. The median patient age was 63 years (IQR 50-72). 71 (10%) of isolates were from blood, 283 (38%) from sputum, 284 (38%) from urine, and 109 (15%) from other specimens. 374 distinct prophage clusters were identified, with significantly more prophages per genome in K pneumoniae (mean 3·01 [SD 1·55]) than in E coli (1·64 [1·46]; p<0·0001). Prophage repertoires largely mirrored bacterial multilocus sequence types. However, even within the highly clonal K pneumoniae sequence type 16 lineage, discrete prophage variation was identified, with common profiles observed in geographically dispersed patients. Respiratory K pneumoniae frequently carried a mosaic prophage with environmental signatures and a type VI secretion system, whereas blood-derived E coli harboured a prophage with immune-modulating genes. Distinct prophage clusters were observed across clinical specimens, age groups, carbapenemase genotype, and geographical region. Strains coharbouring blaNDM-1 plus blaOXA-232 (114 [15%] of 747) had the highest prophage loads. INTERPRETATION: The prophage content was shaped by the bacterial lineage, ecological niche, and temporal dynamics, providing an additional layer of epidemiological resolution beyond conventional genome typing. Integrating prophage profiling into molecular surveillance frameworks could help to identify transmission events, improve infectious source attribution, and enhance infection control strategies. FUNDING: Japan Agency for Medical Research and Development.
Female↗
Prophages and bacterial genomics: what have we learned so far?
Bacterial genome nucleotide sequences are being completed at a rapid and increasing rate. Integrated virus genomes (prophages) are common in such genomes. Fifty-one of the 82 such genomes published to date carry prophages, and these contain 230 recognizable putative prophages. Prophages can constitute as much as 10-20% of a bacterium's genome and are major contributors to differences between individuals within species. Many of these prophages appear to be defective and are in a state of mutational decay. Prophages, including defective ones, can contribute important biological properties to their bacterial hosts. Therefore, if we are to comprehend bacterial genomes fully, it is essential that we are able to recognize accurately and understand their prophages from nucleotide sequence analysis. Analysis of the evolution of prophages can shed light on the evolution of both bacteriophages and their hosts. Comparison of the Rac prophages in the sequenced genomes of three Escherichia coli strains and the Pnm prophages in two Neisseria meningitidis strains suggests that some prophages can lie in residence for very long times, perhaps millions of years, and that recombination events have occurred between related prophages that reside at different locations in a bacterium's genome. In addition, many genes in defective prophages remain functional, so a significant portion of the temperate bacteriophage gene pool resides in prophages.
Base Sequence↗
CTX prophages in classical biotype Vibrio cholerae: functional phage genes but dysfunctional phage genomes.
CTXphi is a filamentous, lysogenic bacteriophage whose genome encodes cholera toxin, the primary virulence factor produced by Vibrio cholerae. CTX prophages in O1 El Tor and O139 strains of V. cholerae are found within arrays of genetically related elements integrated at a single locus within the V. cholerae large chromosome. The prophages of O1 El Tor and O139 strains generally yield infectious CTXphi. In contrast, O1 classical strains of V. cholerae do not produce CTXphi, although they produce cholera toxin and they contain CTX prophages integrated at two sites. We have identified the second site of CTX prophage integration in O1 classical strains and characterized the classical prophage arrays genetically and functionally. The genes of classical prophages encode functional forms of all of the proteins needed for production of CTXphi. Classical CTX prophages are present either as solitary prophages or as arrays of two truncated, fused prophages. RS1, a genetic element that is closely related to CTXphi and is often interspersed with CTX prophages in El Tor strains, was not detected in classical V. cholerae. Our model for CTXphi production predicts that the CTX prophage arrangements in classical strains will not yield extrachromosomal CTX DNA and thus will not yield virions, and our experimental results confirm this prediction. Thus, failure of O1 classical strains of V. cholerae to produce CTXphi is due to overall deficiencies in the structures of the arrays of classical prophages, rather than to mutations affecting individual CTX prophage genes.
Bacteriophages↗
Induction of multiple prophages from a marine bacterium: a genomic approach.
Approximately 70% of sequenced bacterial genomes contain prophage-like structures, yet little effort has been made to use this information to determine the functions of these elements. The recent genomic sequencing of the marine bacterium Silicibacter sp. strain TM1040 revealed five prophage-like elements in its genome. The genomes of these prophages (named prophages 1 to 5) are approximately 74, 30, 39, 36, and 15 kb long, respectively. To understand the function of these prophages, cultures of TM1040 were treated with mitomycin C to induce the production of viral particles. A significant increase in viral counts and a decrease in bacterial counts when treated with mitomycin C suggested that prophages were induced from TM1040. Transmission electron microscopy revealed one dominant type of siphovirus, while pulsed-field gel electrophoresis demonstrated two major DNA bands, equivalent to 35 and 75 kb, in the lysate. PCR amplification with primer sets specific to each prophage detected the presence of prophages 1, 3, and 4 in the viral lysate, suggesting that these prophages are inducible, but not necessarily to the same level, while prophages 2 and 5 are likely defective or non-mitomycin C-inducible phages. The combination of traditional phage assays and modern microbial genomics provides a quick and efficient way to investigate the functions and inducibility of prophages, particularly for a host harboring multiple prophages with similar sizes and morphological features.
Bacteriophages↗
Extensive hidden prophage diversity in Enterobacter species reveals host specificity and local distribution.
Bacteriophages are key drivers of bacterial evolution, particularly through their integration as prophages within host genomes. However, the diversity and host specificity of prophages in relevant pathogens such as Enterobacter species remain poorly characterized. In this study, we revealed the diversity of prophages, mapped their distribution and explored their relationships with their bacterial hosts. We analysed 3,661 prophage sequences identified from the genomes of 20 different Enterobacter species. This analysis uncovered an extensive hidden diversity, comprising 1,617 phage genera and 2,423 phage species - nearly 80% of which were singletons - highlighting an exceptionally rich prophage landscape. We found substantial variation in prophage species richness across host species and isolation sources, with Enterobacter kobei and environmental isolates exhibiting the highest richness. Prophage populations showed strong host specificity and limited cross-species transmission. Moreover, prophages exhibited geographic structuring and significant congruence between host and prophage phylogenies, as well as with the ecological lifestyles of their bacterial hosts. Although we found phages of the same species infecting different host species, these events were infrequent. Finally, bacterial genomes encoded diverse defence systems, mainly PDC-S07, RM type I-II and gabija, whereas only 8.9% of prophages encoded anti-defence systems, mostly anti-CBASS and anti-RM. Overall, this study provides new insights into the diversity of Enterobacter prophages and underscores their ecological and clinical relevance in shaping host adaptation and phage-host dynamics.
Prophages↗
Distribution of prophages and SGI-1 antibiotic-resistance genes among different Salmonella enterica serovar Typhimurium isolates.
Recently, the authors identified Salmonella enterica serovar Typhimurium (S. Typhimurium) definitive type (DT)104-specific sequences of mainly prophage origin by genomic subtractive hybridization. In the present study, the distribution of the prophages identified, ST104 and ST64B, and the novel prophage remnant designated prophage ST104B, was tested among 23 non-DT104 S. Typhimurium isolates of different phage types and 19 isolates of the DT104 subtypes DT104A, DT104B low and DT104L, and the DT104-related type U302. The four S. Typhimurium prophages Gifsy-1, Gifsy-2, Fels-1 and Fels-2 were also included. Analysis of prophage distribution in different S. Typhimurium isolates may supply additional information to enable development of a molecular method as an alternative to phage typing. Furthermore, the presence of the common DT104 antibiotic resistance genes for the penta-resistance type ACSSuT, aadA2, floR, pse-1, sul1 and tet(G), was also studied because of the authors' focus on this emerging type. Based on differences in prophage presence within their genome, it was possible to divide S. Typhimurium isolates into 12 groups. Although no clear relationship was found between different phage type and prophage presence, discrimination could be made between the different DT104 subtypes based on diversity in the presence of prophages ST104, ST104B and ST64B. The novel prophage remnant ST104B, which harbours a homologue of the Escherichia coli O157 : H7 HldD LPS assembly-related protein, was identified only in the 14 DT104L isolates and in the DT104-related U302 isolate. In conclusion, the presence of the genes for penta-resistance type ACSSuT, the HldD homologue containing ST104 prophage remnant and phage type DT104L are most likely common features of the emerging subtype of S. Typhimurium DT104.
Drug Resistance, Bacterial↗
Molecular analysis of the rstR and orfU genes of the CTX prophages integrated in the small chromosomes of environmental Vibrio cholerae non-O1, non-O139 strains.
The ctxAB genes encoding cholera toxin, reside in the genome of a filamentous bacteriophage CTXphi. The presence of CTX prophage in non-epidemic environmental Vibrio cholerae strains is rare. The CTX prophage, the lysogenic form of CTXphi in V. cholerae, is comprised of the 'RS2' and the 'Core'. Analysis of the rstR gene present in the RS2 region of the CTX prophage revealed the presence of new alleles of the prophages in four environmental non-O1, non-O139 strains VCE22 (O36), VCE228 (O27), VCE232 (O4) and VCE233 (O27), and the CTX prophages are located in the small chromosomes. Phylogenetic analysis based on the nucleotide sequences of the rstR and orfU (present in the core) genes of these prophages placed them in a single unique cluster, which is distally located compared with that of epidemic V. cholerae O1 strains. Further analysis indicated that the genome of the prophage present in the strain VCE22 is devoid of the ctxAB genes, called pre-CTX prophage and the strain also possess the toxin-coregulated pilus protein coding gene tcpA of classical type, another important pathogenicity determining locus of the epidemic V. cholerae strains. Comparative analysis of the nucleotide sequences of the rstR and orfU genes indicated that the pre-CTX prophage of VCE22 might be the progenitor of new alleles of the CTX prophages present in these environmental strains.
Bacterial Proteins↗
The Bacillus anthracis chromosome contains four conserved, excision-proficient, putative prophages.
BACKGROUND: Bacillus anthracis is considered to be a recently emerged clone within the Bacillus cereus sensu lato group. The B. anthracis genome sequence contains four putative lambdoid prophages. We undertook this study in order to understand whether the four prophages are unique to B. anthracis and whether they produce active phages. RESULTS: More than 300 geographically and temporally divergent isolates of B. anthracis and its near neighbors were screened by PCR for the presence of specific DNA sequences from each prophage region. Every isolate of B. anthracis screened by PCR was found to produce all four phage-specific amplicons whereas none of the non-B. anthracis isolates, produced more than one phage-specific amplicon. Excision of prophages could be detected by a PCR based assay for attP sites on extra-chromosomal phage circles and for attB sites on phage-excised chromosomes. SYBR-green real-time PCR assays indicated that prophage excision occurs at very low frequencies (2 x 10(-5) - 8 x 10(-8)/cell). Induction with mitomycin C increased the frequency of excision of one of the prophages by approximately 250 fold. All four prophages appear to be defective since, mitomycin C induced culture did not release any viable phage particle or lyse the cells or reveal any phage particle under electron microscopic examination. CONCLUSION: The retention of all four putative prophage regions across all tested strains of B. anthracis is further evidence of the very recent emergence of this lineage and the prophage regions may be useful for differentiating the B. anthracis chromosome from that of its neighbors. All four prophages can excise at low frequencies, but are apparently defective in phage production.
Attachment Sites, Microbiological↗
Chromosomal relocation of prophage-associated bacterial genes.
Taylor, M. W. (Stanford University, Stanford, Calif.), and C. Yanofsky. Chromosomal relocation of prophage-associated bacterial genes. J. Bacteriol. 91:1469-1476. 1966.-Two distinguishable colony types, rough-edged and smooth-edged, were observed when tryptophan auxotrophs of Escherichia coli were transformed to tryptophan independence with DNA from the hybrid nondefective transducing phage i(lambda)h(phi80)T(1) (S)tryp A(+)B(+), and with the helper phage lambdai(434). P1kc transduction experiments with cells of the two types of colonies as genetic donors showed that the i(lambda)h(phi80)T(1) (S)tryp A(+)B(+) prophage was located at different regions of the E. coli chromosome. In cells of rough-edged colonies, the prophage was linked to the tryp-cys region, its normal location, whereas in cells of smooth-edged colonies the prophage was associated with the gal region. When transformation experiments were performed with a T(1) (R)tryp(-) deletion mutant as recipient, and phage lambdai(434) as helper, prophage localization was only detected at the gal region. Localization of (lambda)h(phi80)T(1) (S)tryp A(+)B(+) prophage near gal does not appear to be due to the formation of a recombinant phage carrying tryp A(+)B(+), but is due to some type of interaction between the genomes of i(lambda)h(phi80)T(1) (S)tryp A(+)B(+) and the helper phage. When conditions comparable to those used in transformation studies were employed in transduction experiments, including the use of helper phage, two classes of transductants with either cys or gal linkage were also observed. To examine whether the location of the prophage on the E. coli chromosome had any effect on the ability of the prophage-associated tryp A(+) and tryp B(+) genes to function or respond to different repression conditions, specific activities of the A and B subunits of tryptophan synthetase specified by the phage genome were measured. Similar values were obtained regardless of the location of the prophage-associated tryp genes. Furthermore, the prophage-associated tryp genes, free from their normal operator region, permitted enzyme formation which was unaffected by repression or derepression conditions.
Chromosome Mapping↗
Early events in the replication of Mu prophage DNA.
To determine whether the early replication of Mu prophage DNA proceeds beyond the termini of the prophage into hose DNA, the amounts of both Mu DNA and the prophage-adjacent host DNA sequences were measured using a DNA-DNA annealing assay after induction of the Mu vegetative cycle. Whereas Mu-specific DNA synthesis began 6 to 8 min after induction, no amplification of the adjacent DNA sequences was observed. These data suggest that early Mu-induced DNA synthesis is constrained within the boundaries of the Mu prophage. Since prophage Mu DNA does not undergo a prophage lambda-like excision from its original site after induction (E. Ljungquist and A. I. Bukhari, Proc. Natl. Acad. Sci. U.S.A. 74:3143--3147, 1977), we propose the existence of a control mechanism which excludes prophage-adjacent sequences from the initial mu prophage replication. The frequencies of the Mu prophage-adjacent DNA sequences, relative to other Escherichia coli genes, were not observed to change after the onset of Mu-specific DNA replication. This suggests that these regions remain associated with the host chromosome and continue to be replicated by the chromosomal replication fork. Therefore, we conclude that both the Mu prophage and adjacent host sequences are maintained in the host chromosome, rather than on an extrachromosomal form containing Mu and host DNA.
Base Sequence↗
Comparative genomics and transcriptional analysis of prophages identified in the genomes of Lactobacillus gasseri, Lactobacillus salivarius, and Lactobacillus casei.
Lactobacillus gasseri ATCC 33323, Lactobacillus salivarius subsp. salivarius UCC 118, and Lactobacillus casei ATCC 334 contain one (LgaI), four (Sal1, Sal2, Sal3, Sal4), and one (Lca1) distinguishable prophage sequences, respectively. Sequence analysis revealed that LgaI, Lca1, Sal1, and Sal2 prophages belong to the group of Sfi11-like pac site and cos site Siphoviridae, respectively. Phylogenetic investigation of these newly described prophage sequences revealed that they have not followed an evolutionary development similar to that of their bacterial hosts and that they show a high degree of diversity, even within a species. The attachment sites were determined for all these prophage elements; LgaI as well as Sal1 integrates in tRNA genes, while prophage Sal2 integrates in a predicted arginino-succinate lyase-encoding gene. In contrast, Lca1 and the Sal3 and Sal4 prophage remnants are integrated in noncoding regions in the L. casei ATCC 334 and L. salivarius UCC 118 genomes. Northern analysis showed that large parts of the prophage genomes are transcriptionally silent and that transcription is limited to genome segments located near the attachment site. Finally, pulsed-field gel electrophoresis followed by Southern blot hybridization with specific prophage probes indicates that these prophage sequences are narrowly distributed within lactobacilli.
Animals↗
Prophage induction by DNA topoisomerase II poisons and reactive-oxygen species: role of DNA breaks.
Various compounds were evaluated for their ability to induce prophage lambda in the Escherichia coli WP2s(lambda) microscreen assay. The inability of a DNA gyrase subunit B inhibitor (novobiocin) to induce prophage indicated that inhibition of the gyrase's ATPase was insufficient to elicit the SOS response. In contrast, poisons of DNA gyrase subunit A (nalidixic acid and oxolinic acid) were the most potent inducers of prophage among the agents examined here. This suggested that inhibition of the ligation function of subunit A, which also has a DNA nicking activity, likely resulted in DNA breaks that were available (as single-stranded DNA) to act as strong SOS-inducing signals, leading to prophage induction. Agents that both intercalated and produced reactive-oxygen species (the mammalian DNA topoisomerase II poisons, adriamycin, ellipticine, and m-AMSA) were the next most potent inducers of prophage. Agents that produced reactive-oxygen species only (hydrogen peroxide and paraquat) were less potent than adriamycin and ellipticine but more potent than m-AMSA. Agents that intercalated but did not generate reactive-oxygen species (actinomycin D) or that did neither (teniposide) were unable to induce prophage, suggesting that intercalation alone may be insufficient to induce prophage. These results illustrate the variety of mechanisms (and the relative effectiveness of these mechanisms) by which agents can induce prophage. Nonetheless, these agents may induce prophage by producing essentially the same type of DNA damage, i.e., DNA strand breaks. The potent genotoxicity of the DNA gyrase subunit A poisons illustrates the genotoxic consequences of perturbing an important DNA-protein complex such as that formed by DNA and DNA topoisomerase.
Amsacrine↗
Mechanism of Haemophilus influenzae transfection by single and double prophage deoxyribonucleic acid.
Whole phages HP1 and HP3, vegetative-phage deoxyribonucleic acid (DNA), and single and tandem double prophage DNA were exposed to ultraviolet radiation and then assayed on a wild-type (DNA repair-proficient) Haemophilus influenzae Rd strain and on a repair-deficient uvr-1 strain. Host cell reactivation (DNA repair) was observed for whole-phage and vegetative-phage DNA but not for single and double prophage DNA. Competent (phage-resistant) Haemophilus parainfluenzae cells were normally transfected with H. influenzae-grown phage DNA and with tandem double prophage DNA but not at all with single prophage DNA. CaCl2-treated H. influenzae suspensions could be transfected with vegetative phage DNA and with double prophage DNA but not with single prophage DNA. These observations support the hypothesis that transfection with single prophage DNA occurs through prophage DNA single-strand insertion into the recipient chromosome (at the bacterial att site) followed by DNA replication and then prophage induction.
Bacteriophages↗
Mycoplasma arthritidis bacteriophage MAV1 prophage integration, deletions, and strain-related polymorphisms.
Temperate bacteriophage MAV1 is found in certain highly virulent strains of Mycoplasma arthritidis. Integration sites, portions of the right and left prophage ends, and flanking DNA from eight prophages in seven M. arthritidis strains were characterized in this study. attb and attp sites conformed for the most part to the consensus sequence TATTTTT, although minor polymorphisms were noted. Prophages were integrated into similar sites in four strains, suggesting that these strains may have had a common ancestor. Two strains had three prophage copies each, and integration sites were identical. Two strains had two copies each. One of these shared two of the integration sites occupied in the three-copy strains, while the other shared one of these sites and harbored a second prophage in a unique site. Integration sites in the two strains with one prophage each were unique. Four MAV1 copies contained extensive substitutions within a region encoding a putative structural protein and the putative repressor protein. A 3-kb fragment was deleted from the right side of two of these copies. It is proposed that polymorphisms within MAV1 prophage integration sites and within the prophages themselves may help to identify phylogenetic relationships among virulent M. arthritidis strains.
Amino Acid Sequence↗