Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30536 (PBS)
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The sensitivity, reproducibility and specificity of an enzyme-linked immunosorbent assay (ELISA) for the defective phage PBS Z1 of Bacillus subtilis have been investigated. It was shown that phages in concentrations between 10(8) and 2.5 X 10(10) particles/ml could be assayed with this method. The coefficient of variation for concentrations between 5 X 10(8) and 5 X 10(9) particles/ml was approx. 10%. From some other Bacillus phages tested, only the defective phages resembling PBS Z1 in morphology were detected efficiently with the ELISA for PBS Z1. A comparison is made between ELISA and other assays for PBS Z1.
J Gen Virol 1979 Sep
PMID:An enzyme-linked immunosorbent assay (ELISA) for PBS Z1, a defective phage of Bacillus subtilis. 11 36

We have isolated a new mutant of Bacillus subtilis temperature sensitive in DNA replication; its properties are those of an initiation mutant. When liquid cultures are shifted to 48 degrees DNA replication is the first macromolecular synthesis that stops, but only after synthesis of the amount of DNA predicted for the completion of one replication round. When spores of the mutant are germinated and shifted to 48 degrees at subsequent times, one round of DNA replication is observed only when the shift occurs between 60 and 100 min; earlier shifts do not allow replication to start, later shifts allow more than one replication. The DNA replicated after a shift to high temperature is enriched in markers close to the terminus. The reinitiation of DNA replication stopped by the high temperature, takes place following a shift to a permissive temperature only if protein synthesis is allowed. Examination of DNA replication following toluene treatment shows that the elongation of DNA chains is not affected at the non-permissive temperature. This mutant is shown by PBS-1 mapping to correspond to a new gene denominated dna P, which is located between the thy A and fur A genes and is distinct from all the mapped dna and rec genes of Bacillus subtilis. The mutation confers to the cells also a deficiency in the ability to be transformed, to be transfected with SPP1 phage DNA, and to survive treatment with methyl-methane sulfonate. These deficiencies, observed at the permissive temperature, are no more temperature dependent than in the parental strain. The ability to perform homologous and heterologous transduction with PBS-1 phage and the sensitivity to ultraviolet radiation or mitomycin C are normal.
Mol Gen Genet 1975
PMID:A new mutant of Bacillus subtilis altered in the initiation of chromosome replication. 81 Jun 58

An immunoadsorbent matrix using antibodies against porcine follicle-stimulating hormone (pFSH), a high heterothyrotropic stimulant in tilapia, was used to purify tilapia thyrotropic hormone (t-TSH) from crude pituitary extracts. A homologous bioassay monitored TSH bioactivity during the purification. Thyroid hormones (thyroxine, T4; triiodothyronine, T3; and reverse triiodothyronine, rT3) and testosterone were measured in vivo in Tilapia nilotica. TSH activity eluted as one major peak at pH 2.8 using a PBS-glycine buffer. The TSH fraction increased plasma T4 and plasma rT3. The potency of tTSH was comparable to that of pituitary extract or its Con A II fraction; however, pFSH was a stronger thyroid stimulant. tTSH had no effect on plasma T3 levels and was free of gonadotropic activity, as indicated by its failure to alter plasma testosterone concentrations. Chromatographic and electrophoretic analyses demonstrated a high degree of purity. Like other vertebrate TSHs, the tTSH appeared to have a subunit structure with a possible microgeneity in one subunit.
Gen Comp Endocrinol 1991 Nov
PMID:Purification of tilapia thyrotropin from a crude pituitary homogenate by immunoaffinity chromatography using a matrix of antibodies against porcine follicle-stimulating hormone. 178 65

Bacillus subtilis strains possessing the trpE30 marker (splitting of the trpE locus and a non-tandem duplication of chromosome segment Ib: purB-tre) when transformed or transduced to tryptophan independence mainly give rise to haploid cells with the genetic structure of strain 168. However, among the Trp+ transformants or transductants about 10% are merodiploid carrying a non-tandem duplication of segment C (trpE-ilvA) while maintaining that of segment Ib. Linkage and segregation studies made it possible to determine their genetic structure, which can be represented by three different maps. In map a the copies of Ib are inverted repeats and one of them is flanked by two direct repeats of segment C; in map b two Ib-C segments are inverted repeats and in map c the copies of C are inverted repeats with one of them flanked by direct repeats of Ib. It is proposed that transition from map a to map b and then to map c, and vice versa, may occur by recombination between inverted repeats of either Ib or C. The merodiploids are unstable, recombination between direct repeats leading to haploid cells of 168-type structure. The models proposed for merodiploid formation call for fusion of two recipient chromosomes mediated by the donor segment and recombination between copies of a DNA sequence of the two chromosomes located in different regions. In the case of PBS-1 mediated transduction the greater length of the donor DNA segment makes it possible to obtain the merodiploids with a single recipient chromosome and this needs only a slight modification of the models. No trpE30+ merodiploids are found in transformation when the recipient carries a deletion of the SP beta prophage, or in transduction when both donor and recipient possess this deletion. These results indicate that the homologous sequences involved may be part of the SP beta prophage or that a sequence of bacterial DNA has a good homology with it.
J Gen Microbiol 1983 Mar
PMID:Bacillus subtilis strains carrying two non-tandem duplications of the trpE-ilvA and the purB-tre regions of the chromosome. 640 84

A mutation causing an alteration in Bacillus subtilis ribosomal protein S4 was mapped by transformation and PBS-1 transduction to a site between aroG and argA, a region of the B. subtilis chromosome not previously demonstrated to contain ribosomal protein genes. The S4 mutation conferred a spore-plus phenotype in a streptomycin-resistant, spore-minus genetic background. The altered protein was detectable by polyacrylamide gel electrophoresis of ribosomal proteins of recombinants scored for the spore-plus phenotype in genetic crosses.
Mol Gen Genet 1984
PMID:Genetic mapping of a mutation causing an alteration in Bacillus subtilis ribosomal protein S4. 642 Jun 47

Three aspects of the adsorption of the defective phage PBS Z1 to Bacillus subtilis 168 Wt have been investigated. These are the kinetics, the number of receptors on the cell wall and the character of these receptors. The reaction constants for the binding of phages onto receptors, for the dissociation of the phage-receptor complex and for the transition from reversible to irreversible binding of the phages were calculated from adsorption curves obtained by an enzyme-linked immunosorbent assay (ELISA). They were 1.8 x 10(-13), 6.7 x 10(-2) and 9.0 x 10(-3) respectively. The maximum number of phages adsorbed per cell was 2700, a number limited by the surface area of the cells. Apart from the receptors on the cell wall, receptors on the cell membrane were found. This was concluded from additional adsorption experiments with stable L-forms and contracted phages. Based on these results, together with data from the literature on bacteriocins, phage ghosts and yeast killer factors, a hypothesis concerning the first stage of killing by defective phages has been formulated.
J Gen Virol 1981 Jan
PMID:Adsorption of the defective phage PBS Z1 to Bacillus subtilis 168 Wt. 679 Jun 68

In order to investigate whether defective phages of Bacillus subtilis killed sensitive bacteria by a lysis from without mechanism, the minimal number of phages required for killing was determined. This figure was found to vary with the m.o.i., giving a value of 1 on extrapolation to an m.o.i. of 0. This excluded lysis from without as the only killing mechanism, although it might play a role at high m.o.i.s. This was confirmed by experiments on leakage of ATP and u.v.-absorbing material, the uptake of oxygen and the effect of the phages on the membrane potential. Apart from a short, initial leakage of ATP, the cell membrane was not affected at low m.o.i.s. These results lead to the conclusion that at low m.o.i.s. the phages acted on a cytoplasmic component. Treatment of defective phages for 10 min at pH 2.5 resulted in breakdown of the phages without complete abolition of the killing activity. The active component, which was shown not to be DNA, could not be isolated from the mixture, but SDS gel electrophoresis of PBS X and a non-killing mutant of this phage suggested that a protein with a mol. wt. of 85000 was involved in killing.
J Gen Virol 1981 Oct
PMID:Effect of defective phages on the cell membrane of Bacillus subtilis and partial characterization of the phage protein involved in killing. 679 49

With the use of two-dimensional gel electrophoresis, the proteins present in a transformation-proficient B. subtilis strain were compared with those present in an isogenic, recombination-deficient strain carrying the recE4 mutation. One protein (molecular weight 45 kD, iso-electric point 5.4) was found to be virtually absent in the recE4 strain. This 45 kD protein is a prominent protein predominantly present in the competent fraction of a competent culture. The synthesis of the protein is substantially stimulated by irradiation with ultraviolet light or treatment with mitomycin C and, to a lesser extent, by treatment with nalidixic acid. Since the protein is also observed in a strain cured for SP beta and carrying non-inducible PBS X, it is unlikely that this protein is a gene product specified by one of these prophages usually present in B. subtilis strain 168. Based on these results we conclude that the 45 kD protein is involved in recombination in B. subtilis.
Mol Gen Genet 1982
PMID:Transformation of Bacillus subtilis competent cells: identification of a protein involved in recombination. 681 34

We have studied the meiotic segregation of a chromosome length polymorphism (CLP) in the yeast Saccharomyces cerevisiae. The neopolymorphism frequently observed within the smallest chromosomes (I, VI, III and IX) is not completely understood. We focused on the analysis of the structure of chromosome I in 88 segregants from a cross between YNN295 and FL100trp. Strain FL100trp is known to carry a reciprocal translocation between the left arm of chromosome III and the right arm of chromosome I. PCR and Southern hybridization analyses were performed and a method for the rapid detection of chromosome I rearrangements was developed. Seven chromosome I types were identified among the 88 segregants. We detected 22 recombination events between homologous chromosomes I and seven ectopic recombination events between FL100trp chromosome III and YNN295 chromosome I. These recombination events occurred in 20 of the 22 tetrads studied (91%). Nine tetrads (41%) showed two recombination events. This showed that homologous recombination involving polymorphic homologues or heterologous chromosomes is the main source of neopolymorphism. Only one of the seven chromosome I variants resulted from a transposition event rather than a recombination event. We demonstrated that a Tyl element had transposed within the translocated region of chromosome I, generating mutations in the 3' LTR, at the border between U5 and PBS.
Mol Gen Genet 2000 May
PMID:Homologous recombination and transposition generate chromosome I neopolymorphism during meiosis in Saccharomyces cerevisiae. 1085 95

Group B coxsackieviruses (CVBs) are a major cause of viral myocarditis and pancreatitis in humans and produce a similar pattern of disease in inbred strains of mice. As there are six strains of CVBs, individuals can be infected with multiple serotypes. This raises the possibility of antibody enhancement of infectivity (AEI) by cross-reactive but non-neutralizing antibody to a different strain from a prior infection. To determine whether AEI plays a role in coxsackievirus pathogenesis, an in vitro system using the murine macrophage cell line J774.1 was tested for enhanced infection when incubated with CVB3 plus anti-CVB2 antibody. Yields of virus were found to increase by 10-50-fold and the percentage of infected cells increased proportionately. The effect was Fc-mediated as F(ab')2 fragments of the antibody could not mediate the effect. To determine whether AEI could also be demonstrated in vivo CVB3 was injected into 5-week-old mice together with mouse polyclonal anti-CVB2. Controls included mice injected with PBS or CVB3 alone. Results showed that the titres of virus in tissues of animals injected with virus plus antibody were 1-2 logs higher than when virus was injected alone. This was accompanied by greater histopathological damage, particularly in the heart. These results have implications for human disease as infection with multiple strains likely occurs during the lifetime of an individual.
J Gen Virol 2002 Feb
PMID:Enhancement of coxsackievirus B3 infection by antibody to a different coxsackievirus strain. 1180 28


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