Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:6.3.4.6 (urease)
7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Molecular cloning and sequencing showed that Mycoplasma gallisepticum, like Mycoplasma capricolum, contains both tRNA(UCA) and tRNA(CCA) genes, while Mycoplasma pneumoniae and Mycoplasma genitalium each appear to have only a tRNA(UCA) gene. Therefore, these mycoplasma species contain a tRNA with the anticodon UCA that can translate both UGA and UGG codons.
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PMID:Evidence that UGA is read as a tryptophan codon rather than as a stop codon by Mycoplasma pneumoniae, Mycoplasma genitalium, and Mycoplasma gallisepticum. 210 12

The nucleotide sequences of the complete set of tRNA species in Mycoplasma capricolum, a derivative of Gram-positive eubacteria, have been determined. This bacterium represents the first genetic system in which the sequences of all the tRNA species have been determined at the RNA level. There are 29 tRNA species: three for Leu, two each for Arg, Ile, Lys, Met, Ser, Thr and Trp, and one each for the other 12 amino acids as judged from aminoacylation and the anticodon nucleotide sequences. The number of tRNA species is the smallest among all known genetic systems except for mitochondria. The tRNA anticodon sequences have revealed several features characteristic of M. capricolum. (1) There is only one tRNA species each for Ala, Gly, Leu, Pro, Ser and Val family boxes (4-codon boxes), and these tRNAs all have an unmodified U residue at the first position of the anticodon. (2) There are two tRNAThr species having anticodons UGU and AGU; the first positions of these anticodons are unmodified. (3) There is only one tRNA with anticodon ICG in the Arg family box (CGN); this tRNA can translate codons CGU, CGC and CGA. No tRNA capable of translating codon CGG has been detected, suggesting that CGG is an unassigned codon in this bacterium. (4) A tRNATrp with anticodon UCA is present, and reads codon UGA as Trp. On the basis of these and other observations, novel codon recognition patterns in M. capricolum are proposed. A comparatively small total, 13, of modified nucleosides is contained in all M. capricolum tRNAs. The 5' end nucleoside of the T psi C-loop (position 54) of all tRNAs is uridine, not modified to ribothymidine. The anticodon composition, and hence codon recognition patterns, of M. capricolum tRNAs resemble those of mitochondrial tRNAs.
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PMID:Codon recognition patterns as deduced from sequences of the complete set of transfer RNA species in Mycoplasma capricolum. Resemblance to mitochondria. 247 13

The effects on the urinary tract after inoculation of Ureaplasma urealyticum into the rat bladder were evaluated and compared to that seen after Mycoplasma hominis, Escherichia coli and Proteus mirabilis inoculation. The inoculation of the urease-producing organisms P. mirabilis and U. urealyticum were associated with the formation of struvite bladder stones and predominantly hyperplastic lesions of the bladder. The P. mirabilis inoculated rats also displayed marked pyelonephritis. A similar but much less pronounced reaction also occurred in the kidneys of some of the U. urealyticum inoculated rats. P. mirabilis could frequently be recultured. In contrast, this was not possible with U. urealyticum, but the organism was detected by scanning electron microscopy 2 weeks after the inoculation. Inoculation of M. hominis was associated with a few mild lesions of the bladder, but inflammatory lesions were not present in the kidneys. The study confirms the potential of Ureaplasma to form struvite stones in rat urinary tract. It also demonstrates that it can induce inflammatory changes in both bladder and kidney of rats without concomitant stone formation.
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PMID:Morphological lesions of the rat urinary tract induced by inoculation of mycoplasmas and other urinary tract pathogens. 267 69

Murine antibody against Mycoplasma pulmonis (Mp) was detected sensitively and specifically in experimentally and naturally infected animals by an enzyme-linked immunosorbent assay (ELISA), using urease conjugated antimurine immunoglobulin. More than 98% of the experimentally infected mice and rats exhibited positive reaction in the ELISA two or more weeks after infection, and the titer remained for a prolonged period (up to one year) after infection. However, we failed to detect antibody in the sera of one-week-postinfected animals. Mice and rats from breeding colonies were tested with the ELISA and compared with isolation of Mp from the respiratory organs. Positive reactions were shown in the ELISA using the sera from 91% of the mice and 98% of the rats from which the organisms were isolated. Conversely, 97% of the mice and 78% of the rats among Mp-free animals showed negative results in the ELISA. The sensitivity and specificity of the complement fixation test, which has been used widely for serodiagnosis of Mp-infection, were apparently lower compared to those of the ELISA. From these results, the ELISA was found to be available for the serodiagnosis of Mp-infection in mice and rats.
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PMID:[Serodiagnosis of Mycoplasma pulmonis infection in mice and rats by an enzyme-linked immunosorbent assay]. 315 91

Mycoplasma capricolum uses two tryptophan codons, the "universal" nonsense codon UGA and the universal codon UGG. The bacterium contains two tryptophan tRNAs, one with anticodon UCA, (U: 2'-O-methyl U derivative), and the other with CCA (5'-C: partially 2'-O-methylated). tRNAUCA would translate codons UGA and probably UGG by wobbling. tRNACCA is much less charged by tryptophan in the cells than tRNAUCA, and the intracellular amount of tRNACCA is 5-10 times lower than that of tRNAUCA. The genes for these two tRNAs are separated by a terminator-like structure in a single operon. In vitro transcription experiments suggest that the predominance of tRNAUCA over tRNACCA results from the attenuation of transcription by this terminator-like structure.
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PMID:Evolutionary dynamics of tryptophan tRNAs in Mycoplasma capricolum. 340 3

Clues to evolution of the genetic code can be found by comparing usage of anticodons in various organisms and organelles. GC content of DNA varies, as a result of directional mutation pressure (AT/GC pressure), especially in bacteria. Low GC in Mycoplasma is accompanied by use of UGA for tryptophan and, in ciliated protozoa, by use of UAA and UAG for glutamine. These are examples of "stop codon capture," which has been preceded by duplication of tRNA genes followed by nucleotide substitutions in their sequences, including mutational changes in their anticodons. Evolutionary changes in the code may have resulted from disappearance of codons and anticodons resulting from GC pressure and from their reappearance when the direction of the pressure was reversed. In this manner, codon UGA and anticodon UCA for tryptophan could have disappeared under GC pressure and reappeared in Mycoplasma under AT pressure. Stop codon UGA may have been the third of the three stop codons to appear, originating from mutations in UAA. Changes in the code are adaptive and nondeleterious. We propose that the number of anticodons has increased and that evolution continued until three existing forms of the universal code were produced: eukaryotic, eubacterial, and the code for halobacteria and methanococci. These three codes are distinguished from each other by their anticodon pattern. The eukaryotic code contains eight INN (ANN) anticodons that have replaced GNN anticodons as a result of AT pressure. Mitochondrial and chloroplast codes have evolved from the eubacterial code through genomic economization and AT pressure, leading to losses of GNN and CNN anticodons.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evolution of anticodons: variations in the genetic code. 345 89

Mycoplasma capricolum was previously found to use UGA instead of UGG as its codon for tryptophan and to contain 75% A + T in its DNA. The codon change could have been due to mutational pressure to replace C + G by A + T, resulting in the replacement of UGA stop codons by UAA, change of the anticodon in tryptophan tRNA from CCA to UCA, and replacement of UGG tryptophan codons by UGA. None of these changes should have been deleterious.
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PMID:A change in the genetic code in Mycoplasma capricolum. 393 37

The fastidious growth requirements of mycoplasmas and ureaplasmas necessitated development of special growth media for them. The 1st mycoplasma was isolated from humans in 1937, and in 1954 a previously unknown mycoplasma was isolated from men with nonspecific urethritis. This organism, Ureaplasma urealyticum, is found most frequently in the genitourinary tract, followed by Mycoplasma hominus. M. fermentans and other mycoplasmas are isolated only rarely. Mycoplasmas and ureaplasmas have been implicated in pelvic inflammatory disease, puerperal infection, septic abortion, low birth weight, nongonococcal urethritis, and prostatisis, as well as spontaneous abortion and infertility, but there are no clinical symptoms pathognomonic of these infections. In spite of clinical suggestions of Mycoplasma or Ureaplasma infection, only a properly obtained specimen evaluatd with the use of selective cultures can lead to unequivocal diagnosis. The cultural characteristics and hence diagnostic procedures for Mycoplasma and Ureaplasma are quite different. Sterile calcium alginate swabs are used for obtaining urethral specimens, while sterile cotton swabs can be used for prostatic or vaginal secretions or semen. The swab should not touch antiseptic solutions, creams, or jellies, and the specimen must not dry out. Urine, if cultured, is best examined after centrifugattion at 600 g. Several different transport media are available. Optimally the specimen should be taken directly to the laboratory and subcultured on arrival. The metabolic activity of Mycoplasmas and Ureaplasmas is used in their detection. A phenol red indicator is added to the medium and the color change to or from yellow to pink indicates metabolic change. The growth medium is supplemented with glucose and phenol red for M. fermentans and arginine and phenol red for M. hominis. After color change is observed, the growth medium is subcultured on solid medium, which is obtained by adding .6-.8% Noble agar to the growth medium. Colonies develop best in an atmosphere of 95% N2 and 5% CO2 and reach approximately 200-300 mcm in diameter. They have a fried-egg appearance. Staining with Dienes stain, use of specific antisera, or incident light fluorescence microscopy are used for identification of the classic mycoplasmas. To isolate ureaplasmas, the specimen is transferred on arrival in the laboratory to urease color test broth U9C. During incubation the presence of Ureaplasma induces a rapid color change usually observable in 24-48 hours. A subculture should be done on fresh U9C broth media and on agar media once a color change is observed. Serologic tests for detection of antibodies to mycoplasmas and ureaplasmas are still in the developmental stage.
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PMID:Diagnosis of genital Mycoplasma and Ureaplasma infections. 402 Jul 82

To study the concrement-forming ability of Ureaplasma urealyticum in the urinary tract, viable and heat-killed ureaplasmas as well as urease and non-urease-producing bacteria were inoculated into the bladder in rats. Viable ureaplasmas, in contrast to heat-killed, caused the formation of bladder stones with a frequency corresponding to urease-producing bacteria (Proteus mirabilis). It was not possible to reculture the inoculated ureaplasmas from the urinary tract. Non-urease producing microorganisms (Escherichia coli and Mycoplasma hominis) only occasionally induced stone formation. The results indicate that U. urealyticum can initiate stone formation, a property that appears to be associated with the urease activity of the organism.
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PMID:Concrement formation in the urinary bladder in rats inoculated with Ureaplasma urealyticum. 404 7

Sorbyl-, benzoyl-, and 3-amino-benzoyl hydroxamic acids inhibited the development of an alkaline pH by T-strain cultures grown in broth containing 0.05% urea and phenol red. The specificity of this urease inhibition was demonstrated by the inhibition, by 10(-4)m sorbyl-hydroxamic acid, of the release of (14)CO(2) from (14)C-urea by washed T-strain mycoplasmas in 4 hr of incubation. Sorbyl-, benzoyl-, and 3-amino-benzoyl hydroxamic acids at a concentration of 10(-3)m markedly inhibited the multiplication of T-strain 354 during 18 hr of incubation; this inhibition was not corrected by thymidine at a concentration of 500 mug per ml. Aurothiomalate was 20 times more inhibitory to Mycoplasma hominis DC-63 than to T-strain 354; equivalent inhibitory concentrations were 50 mug per ml for M. hominis and 1,200 mug per ml for T strains.
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PMID:Inhibition of growth of T-strain mycoplasmas by hydroxamic acids and by aurothiomalate. 420 56


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