[The proportion of Escherichia infections caused by enteropathogenic Escherichia and their clinical characteristics in children].
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Child, Preschool↗
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Results for “ESCHERICHIA INFECTIONS”
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Ineffectiveness of rifampicin in inhibiting RNA synthesis in Escherichia coli and T(4)-infected Escherichia coli cells after exposure to ultraviolet radiation.
Resdiual RNA synthesis in Escherichia coli cells and T(4)-infected E. coli cells exposed to ultraviolet radiation is insensitive to rifampicin. On the other hand, residual RNA synthesis in these cells after gamma irradiation is further inhibited by rifampicin. The specific effect exerted by ultraviolet irradiation on transcription seems to arise from alterations in the DNA structure rather than in bacterial RNA polymerase since RNA synthesis in ultraviolet-irradiated E. coli cells infected with unirradiated T(4) is sensitive to rifampicin.
Coliphages↗
Excision of thymine dimers in vitro by extracts of bacteriophage-infected Escherichia coli.
Extracts of DNA polymerase I defective Escherichia coli infected with phage T4 contain an exonuclease activity that removes thymine dimers from UV-irradiated DNA previously nicked with T4 UV endonuclease. This activity is not expressed if cells are infected in the presence of chloramphenicol. The enzyme has a requirement for divalent cation and is not affected by caffeine, but excision is inhibited in the presence of proflavine. The enzyme is present in all phage T4 mutants thus far examined, including 25 UV-sensitive mutants isolated during the course of the experiments, all of which are defective in the v gene. A similar activity can be detected in cells infected with phages T2, T3, and T6, but not in cells infected with phage T7.
Caffeine↗
Zinc uptake and incorporation into proteins in T4D bacteriophage-infected Escherichia coli.
The metabolism of Zn2+ in Escherichia coli infected with T4D bacteriophage and various T4D mutants has been examined. E. coli B infected with T4D, and all T4D mutants except T4D 12-, took up zinc ions at a rate identical to that of uninfected cells. E. coli B infected with T4D 12- had a markedly decreased rate of zinc uptake. The incorporation of zinc into proteins of infected cells has also been studied. T4D phage infection was found to shut off the synthesis of all bacterial host zinc metalloproteins while allowing the formation of viral-induced zinc proteins. The amount of zinc incorporated into viral proteins was affected by the absence of various T4D gene products. Cells infected with T4D 12-, and to a much less extent those infected with T4D 29-, incorporated the least amount of zinc into proteins, while cells infected with T4D 11- and T4D 51- incorporated increased amounts of zinc into the zinc metalloproteins. In cells infected with T4D 11- and 51- most of the zinc protein was found to be the product of gene 12. The marked effect of infection of E. coli with T4D 12- on both zinc uptake and zinc incorporation into protein supports the conclusion that T4D gene 12 protein is a zinc metalloprotein. Additionally, these observations have indicated that this metalloprotein interacts with host cell membrane.
Biological Transport↗
Synthesis of bacteriophage and host DNA in toluene-treated cells prepared from T4-infected Escherichia coli: role of bacteriophage gene D2a.
We investigated the synthesis of DNA in toluene-treated cells prepared from Escherichia coli infected with bacteriophage T4. If the phage carry certain rII deletion mutations, those which extend into the nearby D2a region, the following results are obtained: (i) phage DNA synthesis occurs unless the phage carries certain DNA-negative mutations; and (ii) host DNA synthesis occurs even though the phage infection has already resulted in the cessation of host DNA synthesis in vivo. The latter result indicates that the phage-induced cessation of host DNA synthesis is not due to an irreversible inactivation of an essential component of the replication apparatus. If the phage are D2a(+), host DNA synthesis in toluene-treated infected cells is markedly reduced; phage DNA synthesis is probably also reduced somewhat. These D2a effects, considered along with our earlier work, suggest that a D2a-controlled nuclease, specific for cytosine-containing DNA, is active in toluene-treated cells.
Coliphages↗
Ribonucleoside and deoxyribonucleoside triphosphate pools during 2-aminopurine mutagenesis in T4 mutator-, wild type-, and antimutator-infected Escherichia coli.
Ribonucleoside and deoxyribonucleoside triphosphate pools have been measured in Escherichia coli infected with bacteriophage T4 DNA polymerase mutator, wild type, and antimutator alleles during mutagenesis by the base analogue 2-aminopurine. ATP and GTP pools expand significantly during mutagenesis, while CTP and UTP pools contract slightly. The DNA polymerase (gene 43) alleles and an rII lesion perturb normal dNTP pools more than does the presence of 2-aminopurine. We find no evidence that 2-aminopurine induces mutations indirectly by causing an imbalance in normal dNTP pools. Rather, it seems likely that, by forming base mispairs with thymine and with cytosine, 2-aminopurine is involved directly in causing bidirectional A.T in equilibrium G.C transitions. The ratios for 2-aminopurine deoxyribonucleoside triphosphate/dATP pools are 5-8% for tsL56 mutator and 1-5% for tsL141 antimutator and 43+ alleles. We conclude that the significant differences observed in the frequencies of induced transition mutations in the three alleles can be attributed primarily to the properties of the DNA polymerases with their associated 3'-exonuclease activities in controlling the frequency of 2-aminopurine.cystosine base mispairs.
2-Aminopurine↗
STUDIES OF URINARY TRACT INFECTIONS IN INFANCY AND CHILDHOOD. IV. RELATION OF THE COLI ANTIBODY TITRE TO CLINICAL PICTURE AND TO SEROLOGICAL TYPE OF THE INFECTING ESCHERICHIA COLI IN ACUTE, UNCOMPLICATED URINARY TRACT INFECTIONS.
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Allergy and Immunology↗
Synthesis of an S-adenosylmethionine-cleaving enzyme in T3-infected Escherichia coli and its disturbance by co-infection with enzymatically incompetent bacteriophage.
Synthesis of an S-adenosylmethionine-cleaving enzyme evoked by infection of Escherichia coli with phage T3 was independent of the multiplicity of infection with the wild type, T3 sam(+). It was depressed, however, by mixed infection with related phages genetically incapable of directing enzyme production, such as T3 sam(-), or phage T7. The depressor effect of enzymatically incompetent genomes depended on their proportion among the input phage and not on their absolute multiplicity. The effect was more pronounced with homologous, enzymatically incompetent phage (T3 sam(-)) than with heterologous phage (T7). After ultraviolet irradiation, enzymatically incompetent genomes lost their depressing power; at a survival level of 10(-7), no depression by either homologous or heterologous phage upon T3 sam(+)-directed enzyme synthesis was detected.
Carbon Isotopes↗
A stereochemical study of the mechanism of activation of donor oligonucleotides by RNA ligase from bacteriophage T4 infected Escherichia coli.
RNA ligase from bacteriophage T4 infected Escherichia coli catalyzes the activation of adenosine 3',5'-bisphosphate (representing the donor oligonucleotide) by adenosine 5'-[(S)-alpha-17O,alpha,alpha-18O2]triphosphate with retention of configuration at P alpha. Since single-step enzyme-catalyzed nucleotidyl transfer reactions proceed with inversion, this stereochemical result provides support for a double displacement mechanism involving an adenylyl-enzyme intermediate as proposed previously from isotope exchange experiments.
Adenine Nucleotides↗
The stereochemical course of phosphoryl transfer catalysed by polynucleotide kinase (bacteriophage-T4-infected Escherichia coli B).
Polynucleotide kinase (bacteriophage-T4-infected Escherichia coli B) catalyses the transfer of the [gamma-16O,17O,18O]phosphoryl group from 5'[gamma(S)-16O,17O,18O]ATP to 3'-AMP with inversion of configuration at the phosphorus atom. The simplest interpretation of this observation is that the [gamma-16O,17O,18O]phosphoryl group is transferred directly from ATP to the co-substrate by an 'in-line' mechanism.
Adenosine Triphosphate↗
Analysis of the baseplate region of phage AR1 that specifically infects Escherichia coli O157:H7.
Phage AR1 that specifically infects Escherichia coli O157:H7 has been characterized previously for its primary host contact molecule, the long tail fiber. To strengthen its attachment to the host bacteria, the phage may use its baseplate for a second contact. This study investigated the characteristics of AR1 baseplate by deducing the responsible genes including wac and genes 9 to 15. The wedge pin g11 and the short tail fiber g12 varied the most, whereas the others were highly conserved compared with their counterparts in T4. The degrees of gene conservation correlated well with the known functions of individual gene products.
Bacteriophage T4↗
Phospholipid metabolism in T4 bacteriophage infected Escherichia coli K-12 (lambda).
Infection of Escherichia coli K-12 (lambda) by bacteriophage results in an altered labeling pattern of phospholipids in the host cell. Although the overall incorporation of (32)P(i) into phospholipids is decreased by infection, the relative amounts of phosphatidylglycerol and cardiolipin are increased. Phospholipid changes occurring at later stages in the lytic cycle of infected bacteria are more prominent than those at earlier time intervals. The uptake of (32)P(i) into phospholipids of cells infected with T4Bs and endolysin-negative mutants was similar to that observed with the wild-type phage, suggesting that the development of resistance to lysis from without and the repair of mucopeptides are not responsible for the phospholipid changes. The metabolism of phospholipids in uninfected cells treated with cyanide was similar to that of infected cells, indicating that part of the phage-induced alterations may be a consequence of impaired respiration.
Chromatography, Thin Layer↗
Transcription in bacteriophage f1-infected Escherichia coli. Messenger populations in the infected cell.
Transcription of bacteriophage f1 DNA in vivo occurs in two independent regions. They are separated from one another by a strong terminator just downstream from gene VIII on one side, and by the filamentous phage intergenic space on the other. One of these regions contains genes II, V, VII, IX and VIII, and is actively transcribed. In this region there are a number of promoters but only one effective terminator. Thus, most of the RNAs that come from this region overlap and share sequences close to the termination site. The other region, which contains genes III, VI, I and IV, is transcribed much less actively. This region gives rise to a long (approximately 4 X 10(3) bases) RNA that covers the entire region, and several RNAs that overlap in the region closest to their 5' termini. Several other RNAs appear to overlap only with the 4 X 10(3) base transcript. Thus, not only the frequency but the organization of transcription differs in the two portions of the genome.
Coliphages↗
F-Factor-mediated restriction of bacteriophage T7: synthesis of RNA and protein in T7-infected Escherichia coli F- and F+ cells.
Bacteriophage T7 is unable to productively infect Escherichia coli strains carrying the sex factor F. T7 phage development, in terms of RNA and protein synthesis, was compared in T7-infected isogenic F- and F+ strains of E. coli. Slightly less T7 early mRNA and early protein were synthesized in F+ cells. In addition to the defect in T7 late protein production in F+ cells reported by others, significantly less T7 late mRNA was synthesized, about one-half of that produced in T7-infected F- cells. Moreover, host RNA synthesis was not completely inhibited. The protein-synthesizing ability of T7-infected F+ cells decayed much faster than that of F- cells both in vivo and in vitro. This faster decay appears to explain the failure of F+ cells to produce T7 late protein in vivo, even in the presence of a considerable amount of translatable T7 late mRNA. Therefore, it may not be necessary to postulate the involvement of specific translational discrimination against T7 late mRNA, although it appears that F-factor-mediated restriction of T7 involves changes in transcription as well as translation.
Cell-Free System↗
Recovery of polysome function of T4-infected Escherichia coli after brief treatment with chloramphenicol and rifampin.
T4-infected Escherichia coli cells briefly exposed to rifampin, or to rifampin plus chloramphenicol, were capable of protein synthesis for some time after removal of the antibiotics, although ribonucleic acid synthesis was irreversibly inhibited. Partially completed peptides trapped on polysomes by high levels of chloramphenicol were eventually completed after removal of the drug, as demonstrated by subjecting labeled peptides from appropriate polysome regions to polyacrylamide disc gel electrophoresis. Thus, the effect of the drug appears to be reversible on the molecular as well as the cellular level.
Chloramphenicol↗
Nonspecific protective action against Vibrio cholerae of SK&F 42319, a ribonucleic acid obtained from bacteriophage-infected Escherichia coli.
An interferon-inducing RNA, SK&F 42319, obtained from a lysate of phage-infected Escherichia coli, protected mice against Vibrio cholerae infection. This nonspecific protection was not attributable to endotoxin contamination.
Animals↗
Deletion between directly repeated DNA sequences measured in extracts of bacteriophage T7-infected Escherichia coli.
An in vitro system based upon extracts of bacteriophage T7 infected Escherichia coli was used to study genetic deletions and to examine the importance of DNA replication in the deletion process. When T7 genomes with gene 1.3 inactivated by a 43-bp insert of random sequence DNA bracketed by 11-bp direct repeats were replicated in vitro the inserts were deleted with a frequency of about 10(-5) deletions per genome replication. Under conditions where deletion could take place only by recombination between direct repeats on distinct DNA molecules deletion frequency was at least an order of magnitude lower. These data demonstrate the utility of the in vitro system as a means for examining deletion mechanisms and underscore the importance of DNA replication in deletions.
Bacteriophage T7↗
In vitro transcription of phage T4 late genes on purified DNA by partially purified RNA polymerase from T4-infected Escherichia coli b cells.
RNA polymerase was purified from 'late' phage T4-infected Escherichia coli B cells by DNA-cellulose affinity chromatography and high salt agarose filtration. The DNA-cellulose-purified RNA polymerase preparation contained T4-coded DNA endonuclease activity and several proteins, some with sizes comparable with the known T4 maturation factors, essential for late RNA synthesis. Some of these proteins, and the DNA endonuclease utilizing native, parental T4 DNA and supercoiled phi X 174 DNA as substrates, were partially separated from the RNA polymerase as a complex during agarose filtration. In vitro RNA was made by the DNA-cellulose-purified RNA polymerase using native, parental T4 DNA as template. About 26% of the in vitro RNA was transcribed from the DNA r-strand; 75% from the same r-strand region as in vivo late after infection. Both the abundancy and specificity of the in vitro r-strand transcription were markedly reduced after agarose filtration of the enzyme. Addition of the proteins separated from the RNA polymerase during agarose filtration caused a restoration of in vitro r-strand transcription abundance, but not its specificity. These results show that partially purified RNA polymerase from T4-infected E. coli B cells was able to transcribe late T4 genes in vitro with some abundancy and specificity on purified, parental T4 DNA, but further purification of the enzyme caused an irreversible reduction of this ability.
Bacterial Proteins↗