Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bordetella bronchiseptica is a respiratory tract pathogen in a variety of species. Previous studies suggest little genetic variation among canine B. bronchiseptica isolates. The degree of genetic diversity in 26 canine B. bronchiseptica strains was evaluated using randomly amplified polymorphic DNA (RAPD) fingerprinting and ribotyping. Strains evaluated include historic reference strains (N=3). vaccine strains (N=5) and clinical isolates (N=18). RAPD fingerprinting with the 10-nucleotide primer OPA-4 resulted in four distinct fingerprint patterns. RAPD fingerprinting consistently separated four previously characterized electromorphotype (EMT) 6 strains into two fingerprint types. Ribotyping, using the restriction endonuclease PvuI, resulted in six distinct ribotypes. With the exception of vaccine strains, considerable genetic diversity exists in the canine B. bronchiseptica isolates examined. These findings indicate the genetic variability within canine strains of B. bronchiseptica is greater than appreciated previously. Additionally, OPA-4 RAPD fingerprinting and PvuI ribotyping will be useful tools in epidemiologic studies of canine B. bronchiseptica isolates.
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PMID:Evaluation of canine Bordetella bronchiseptica isolates using randomly amplified polymorphic DNA fingerprinting and ribotyping. 1022 21

Fifty-seven bacterial isolates previously identified as Bordetella avium or B. hinzii were characterized by restriction enzyme analysis (REA) and/or ribotyping. Twenty restriction endonucleases were evaluated for REA. Digestion of chromosomal DNA from the 42 B. avium and 15 B. hinzii isolates with HinfI produced 8 and 7 distinct fingerprint profiles, respectively. Digestion with DdeI further discriminated these Bordetella species and produced 12 fingerprint profiles for B. avium and 4 profiles of B. hinzii. In addition, B. avium isolates were clearly distinguishable from B. hinzii isolates by ribotyping with the restriction endonuclease PvuII. The ribotype patterns of these two species of Bordetella were unique when compared to previously reported ribotype patterns for B. bronchiseptica isolates. Since it was possible to discern differences among isolates within each Bordetella species by REA analysis, we suggest that REA could be used in developing a typing system based on the fingerprint profiles generated.
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PMID:Restriction enzyme analysis and ribotyping distinguish Bordetella avium and Bordetella hinzii isolates. 1072 34

The goal of the present study was to characterize, by ribotyping and restriction endonuclease analysis (REA), 35 phocine Bordetella bronchiseptica isolates and to ascertain their relationship to one another and to isolates acquired from other host species. Thirty-four isolates were obtained in Scotland during a 10-year period encompassing the 1988 epizootic; the remaining isolate was obtained independently in Denmark. All phocine isolates had an identical Pvu II ribotype unique from the 18 ribotypes previously detected in strains from heterologous hosts. Alternative restriction enzymes, useful for subgrouping strains within Pvu II ribotypes, also failed to discriminate among isolates from seals. The exclusive occurrence of a single ribotype of B. bronchiseptica in a particular host species has not been previously observed. Similarly, REA based on either HinfI or Dde I profiles did not reveal detectable polymorphisms, although unique patterns were readily distinguished among a limited number of isolates from other host species. This is the first report demonstrating the utility of REA using frequently cutting enzymes for discrimination of B. bronchiseptica strains. These data suggest that B. bronchiseptica-induced respiratory disease in seals along the Scottish shore may be due to the circulation of a single, unique clone.
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PMID:Ribotyping and restriction endonuclease analysis reveal a novel clone of Bordetella bronchiseptica in seals. 1110 53

Bordetella avium is an avian respiratory disease pathogen responsible for substantial economic losses to the turkey industry. The inability to distinguish isolates has hampered outbreak investigations and prevents a complete understanding of transmission mechanisms. Isolates of Bordetella hinzii, often referred to as B. avium-like or as Alcaligenes faecalis type II prior to 1995, have also been acquired from the respiratory tracts of diseased poultry but are not believed to be pathogenic for birds. Therefore, differentiating between B. avium and B. hinzii is of importance for veterinary diagnostic laboratories. It was recently reported that both PvuII ribotyping and HinfI/DdeI restriction endonuclease analysis (REA) show promise for distinguishing isolates of B. avium and B. hinzii. Here we compare the ability of these techniques to discern inter- and intraspecies differences. While both approaches distinguished numerous types within a species, only REA was sufficiently discriminatory for routine use as an epidemiologic tool. Both techniques clearly distinguish between B. avium and B. hinzii, although the results of ribotyping are more easily interpreted. Ribotyping and REA identified numerous, previously unrecognized B. hinzii strains from a collection of bordetella isolates, including one acquired from a rabbit. This is the first report of B. hinzii isolation from a nonhuman mammalian species. At least some of the newly recognized B. hinzii isolates have been previously reported to cause disease in poults, suggesting that the pathogenicity of this agent for poultry should be more rigorously examined.
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PMID:Comparison of ribotyping and restriction enzyme analysis for inter- and intraspecies discrimination of Bordetella avium and Bordetella hinzii. 1268 38

The degree of genetic diversity in 45 Bordetella (B.) bronchiseptica strains comprised of a vaccine strain (N = 1), reference strains (N = 3) and field isolates (N = 41) was evaluated using random amplified polymorphic DNA (RAPD) fingerprinting and pulsed-field gel electrophoresis (PFGE). Three candidate primers were selected for RAPD analysis after screening 20 random decamer oligonucleotides for their discriminatory abilities. The OPA-07, OPA-08 and OPA-18 primers yielded 10, 10, and 6 distinct fingerprint patterns, respectively. The most common identical RAPD pattern was produced by OPA-07 which was shared by 32 isolates (71.1%), the pattern produced by OPA-08 was shared by 26 isolates (57.8%), and the pattern produced by OPA-18 was shared by 40 isolates (88.9%). The RAPD patterns of the vaccine strain and the 3 reference strains did not match any of the patterns produced by the field isolates when primers OPA-07 and OPA-08 were used. PFGE using the restriction endonuclease XbaI produced a total of 15 patterns consisting of 4 PFGE types (A, B, B1 and C, differing by > or = 4 bands) and 11 A subtypes (differing by < or = 3 bands). Most of the field isolates exhibited identical type A and B patterns, suggesting that they were related. The vaccine strain and the three reference strains showed different PFGE patterns as compared to the identical type A strains.
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PMID:Diversity of swine Bordetella bronchiseptica isolates evaluated by RAPD analysis and PFGE. 1732 76

Plasmids, conjugative transposons and phage frequently encode anti-restriction proteins to enhance their chances of entering a new bacterial host that is highly likely to contain a Type I DNA restriction and modification (RM) system. The RM system usually destroys the invading DNA. Some of the anti-restriction proteins are DNA mimics and bind to the RM enzyme to prevent it binding to DNA. In this article, we characterize ArdB anti-restriction proteins and their close homologues, the KlcA proteins from a range of mobile genetic elements; including an ArdB encoded on a pathogenicity island from uropathogenic Escherichia coli and a KlcA from an IncP-1b plasmid, pBP136 isolated from Bordetella pertussis. We show that all the ArdB and KlcA act as anti-restriction proteins and inhibit the four main families of Type I RM systems in vivo, but fail to block the restriction endonuclease activity of the archetypal Type I RM enzyme, EcoKI, in vitro indicating that the action of ArdB is indirect and very different from that of the DNA mimics. We also present the structure determined by NMR spectroscopy of the pBP136 KlcA protein. The structure shows a novel protein fold and it is clearly not a DNA structural mimic.
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PMID:The structure of the KlcA and ArdB proteins reveals a novel fold and antirestriction activity against Type I DNA restriction systems in vivo but not in vitro. 2000 96


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