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)

Three California turkey premises that had repeated outbreaks of fowl cholera were studied for periods of 2 to 4 years. Using biochemical, serologic, plasmid DNA, and restriction endonuclease analyses of isolates of Pasteurella multocida from turkeys and wildlife on the premises, strains of the organism were found to be enzootic on two of the premises. On the third, a variety of strains of P. multocida were isolated from fowl cholera outbreak flocks.
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PMID:Restriction endonuclease analysis of Pasteurella multocida isolates from three California turkey premises. 162 99

Restriction endonuclease analysis (REA) of whole-cell DNA was used to determine possible sources of Pasteurella multocida for each outbreak of fowl cholera occurring in turkey flocks in eight commercial poultry companies in California from October 1988 to September 1989. Over this period, 179 isolates of P. multocida were obtained from dead turkeys in 80 meat and breeder flocks on 43 premises. P. multocida was isolated from wildlife on five premises. Isolates were characterized by subspecies, serotype, presence of plasmid DNA, and REA type. In 52 (65%) flocks, all isolates of P. multocida had the same REA pattern as the M9 live vaccine strain following digestion of DNA with the restriction enzyme SmaI. Field strains of P. multocida were obtained from 27 (34%) flocks, and one flock (1%) yielded both M9 and a field strain of the organism. REA of field strains of P. multocida revealed 17 different SmaI REA types. Based on matching SmaI REA types, potential sources of P. multocida were identified for 15 of the 28 flocks infected with field strains of the organism, and transmission between turkey premises was a possibility in only seven flocks.
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PMID:Transmission of Pasteurella multocida on California turkey premises in 1988-89. 162 98

When activated with either Con A, a CD3-specific mAb, or Ag-pulsed B lymphoma (LK35.2) cells, CD4 (Th1) clones quickly induce DNA fragmentation in target cells followed by release of 51Cr-labeled intracellular materials. Both activated CD4 clones and CD8 (CTL) cells fragment target DNA into electrophoretically identical "ladder" pattern made of approximately 200 bp. The effect of various metabolic inhibitors on the ability of CD4 and CD8 cells to induce target DNA fragmentation was studied. Little effect was observed with the DNA synthesis inhibitor, mitomycin C. The RNA synthesis inhibitor, actinomycin D, and the protein synthesis inhibitor, cycloheximide, strongly inhibited the ability of CD4 cells, but not CD8 cells, to induce target DNA fragmentation. In contrast, target DNA fragmentation by CD8 cells, but not by CD4 cells, was inhibited by cholera toxin. Although cyclosporin A inhibited CD4 cells to fragment target DNA during the early phase (90 min) of E:T interaction, this inhibition was not sustained in the later phase (210 min) of the assay. Zinc ions inhibited the ability of both CD4 and CD8 cells to fragment target DNA. Treatment of effectors and targets with these inhibitors, followed by washings, demonstrated that the action of these inhibitors on effector cells alone is sufficient to inhibit target DNA fragmentation. The strong correlation among these parameters of DNA fragmentation and Cr-release assays supports the hypothesis of programed cell death. Although distinct cytolytic pathways are used by CD4 and CD8 cells to kill targets, both pathways deliver a signal that activates endonuclease(s), fragments target DNA, causes Cr-release, and lyses target cells. Taken together with our previous studies, the present findings demonstrate that activated cytolytic CD4 clones do not use perforin, serine proteases, and TNF as mediators for resistant target DNA fragmentation.
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PMID:Distinct pathways of CD4 and CD8 cells induce rapid target DNA fragmentation. 167 Oct 51

The gene encoding a hemolysin similar to the thermostable direct hemolysin (TDH) of Vibrio parahaemolyticus was previously cloned from a plasmid of Vibrio cholerae non-O1. The gene (designated as NAG-tdh) was subcloned and its nucleotide sequence was determined and compared with reported sequences of the four tdh gene copies encoding TDH, of which three were cloned from the chromosome and one was cloned from a plasmid of V. parahaemolyticus. In the coding region, the NAG-tdh gene had 100% homology with the plasmid-borne tdh gene (tdh4) whereas the NAG-tdh gene was 96.7-98.6% homologous to the three chromosomal tdh genes. The sequences of the NAG-tdh and tdh4 genes were nearly identical in the further upstream and downstream regions. The entire plasmids carrying the two tdh genes were found to be highly homologous when compared by restriction endonuclease and Southern blot analyses. The results suggest that the tdh gene has been transferred between V. cholerae non-O1 and V. parahaemolyticus by a plasmid, directly or indirectly, and that the nucleotide sequences of the tdh gene-bearing plasmids have undergone minor base changes in the respective genetic backgrounds.
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PMID:Similarity of the tdh gene-bearing plasmids of Vibrio cholerae non-O1 and Vibrio parahaemolyticus. 185 99

Enterotoxigenic strains of Vibrio cholerae O-1 biotype eltor, isolated from three sporadic cases of cholera in Nagoya in 1989 and an outbreak of cholera in Nagoya in 1989 were analyzed for their similarities. All isolates of V. cholerae O-1 were indistinguishable in bacteriophage types, serovars, biovars and drug resistance patterns. Because the epidemiological investigation based on a primary structure of chromosomal DNA is more reliable, we isolated chromosomal DNA from these isolates and compared electrophoretic patterns of restriction endonuclease-digested DNA fragments. Furthermore, Southern hybridization of the cholera toxin gene was performed. Since no difference among six strains in these sporadic was observed, it was strongly suggested that both the independent cases and the outbreak of cholera were caused by the same strain.
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PMID:[Molecular epidemiology of Vibrio cholerae O-1 from outbreak and sporadic patients in Nagoya in 1989]. 191 14

Wildlife isolates of Pasteurella multocida, whose virulence for turkeys had previously been determined by intravenous inoculation, were characterized regarding their ability to survive incubation in fresh non-immune turkey serum. The relative virulence of the isolates was significantly associated with their ability to resist the bactericidal power of the serum as determined by standard plate counts following incubation. Organisms with a high survival value were more virulent; those with a low survival value were less virulent. A statistical model was specified and was successfully used to predict relative virulence of the P. multocida isolates. This method of assaying serum resistance was rapid, repeatable, and practical and could be performed with minimal laboratory equipment. Also studied was the serum resistance of seven serotype 3, 4 isolates obtained from the lungs of M9-vaccinated turkeys from seven flocks experiencing increased mortality due to fowl cholera. These isolates were shown to be identical to the M9 vaccine by restriction endonuclease analysis of chromosomal DNA. Six of the seven isolates had higher serum survival values than the original M9 vaccine.
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PMID:Serum resistance as an indicator of virulence of Pasteurella multocida for turkeys. 228 18

Fifty-five serotype 3,4 isolates of Pasteurella multocida, isolated from turkeys dead from fowl cholera, were characterized (fingerprinted) genotypically for comparison with the serotype 3,4 live fowl cholera vaccine principally used in turkeys in California. Twenty-three isolates were obtained from turkeys vaccinated with the M9 live vaccine, and 32 additional isolates were from turkeys not vaccinated for fowl cholera. Methods of characterization included restriction endonuclease analysis of chromosomal DNA and ribotyping, a technique for highlighting restriction site heterogeneity of highly conserved ribosomal RNA genes and associated sequences using a radiolabeled rRNA probe. Eight different genotypes or ribotypes were detected in these isolates by the above methods. Of 23 isolates from M9-vaccinated turkeys flocks, 19 were the same ribotype as M9. Thirty of 32 isolates recovered from unvaccinated turkeys were different ribotypes from M9. The remaining two isolates resembled M9 and were recovered from two different flocks placed in succession on a turkey farm where a flock placed previously had been vaccinated with M9, suggesting interflock transmission. Ribotyping and restriction endonuclease analysis appear to be useful tools to aid in the determination of the role that the live vaccine plays in fowl cholera epidemiology.
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PMID:Differentiation of field isolates of Pasteurella multocida serotype 3,4 from live vaccine strain by genotypic characterization. 236 81

The artificially synthesized aquatic Aeromonas hydrophila partial aerolysin gene DNA (Ae, containing 48 oligonucleotides), and partial cholera-toxin gene DNA fragments (C1 and C2, containing 34 and 19 oligonucleotide, respectively) were used as probes to determine their DNA sequence homology to the chromosome DNA of 191 strains of the clinically isolated A. hydrophila, using the colony hybridization test. The three probes had a positive reaction with clinical A. hydrophila strains. Several positive strains of this organism were further screened by cutting reaction with restriction endonuclease BamHI and EcoRI, the alkaline Southern transfer, and DNA hybridization test. Some strains were found to be positive in reacting with Ae and C1, but negative with C2. The findings led to the conclusion that the DNA sequences were homologous among the clinical A. hydrophila toxin gene, cholera-toxin gene and aquatic A. hydrophila aerolysin gene.
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PMID:[Clinical Aeromonas hydrophila contain the DNA fragments with nucleotide sequence similar to those of hemolysin and cholera-toxin gene]. 239 87

Two hundred and eight strains of Vibrio cholerae serovar O1 and 454 non-O1 strains, which were isolated within or imported into Australia, were tested for the production of cholera enterotoxin and for hybridization with gene probes for cholera enterotoxin. Genetic relationships among representative isolates were studied by a comparison of the restriction-endonuclease digest patterns of the chromosomal DNA and by Southern-blot analysis of toxigenic strains with the cholera-toxin gene probe. V. cholerae O1 isolates from patients and from the environment were predominantly toxigenic in contrast with the non-O1 isolates. The local O1 isolates were found to be diverse genetically and were unrelated to the imported O1 isolates, to those from other endemic areas and to non-O1 isolates.
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PMID:A molecular epidemiological study of Vibrio cholerae in Australia. 254 36

The Hly region from the chromosome of Vibrio cholerae El Tor strain RV79(Hly-) and the nonhemolytic classical strain 569B were cloned into plasmid vector pBR322. Escherichia coli K-12 transformants possessing these recombinant plasmids were nonhemolytic and were detected with a 32P-labeled hly-specific DNA probe. Restriction endonuclease Sau3AI digestions of the cloned hly loci of two independently obtained RV79(Hly+) convertants, when compared with the digests of cloned RV79(Hly-) loci, revealed that an apparent alteration (10 to 15 base pairs) had occurred. In contrast, an apparent 20-base-pair deletion was present in the cloned hly locus of the classical biotype V. cholerae strain 569B. Maxicell analysis and immunoprecipitation of labeled proteins of E. coli which are encoded by the cloned hly loci of RV79(Hly+) and from nuclease BAL 31-deleted plasmids, as well as immunoprecipitation of [35S]methionine-labeled V. cholerae proteins, suggest that the hemolysin is an 84,000-dalton polypeptide.
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PMID:Cloning and characterization of the hemolysin determinants from Vibrio cholerae RV79(Hly+), RV79(Hly-), and 569B. 257 40


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