5-Fluorouracil-resistant strain of Methanobacterium thermoautotrophicum
| Autor: | A Eisenbraun, R Teal, D P Nagle |
|---|---|
| Rok vydání: | 1987 |
| Předmět: |
chemistry.chemical_classification
Pyrimidine Strain (chemistry) Wild type Uracil phosphoribosyltransferase activity Drug Resistance Microbial Uracil Euryarchaeota Biology Microbiology Pyrimidine analogue chemistry.chemical_compound chemistry Biochemistry Nucleic acid Nucleotide Fluorouracil Pentosyltransferases Molecular Biology Research Article |
| Zdroj: | Journal of Bacteriology. 169:4119-4123 |
| ISSN: | 1098-5530 0021-9193 |
| DOI: | 10.1128/jb.169.9.4119-4123.1987 |
| Popis: | Growth of Methanobacterium thermoautotrophicum Marburg is inhibited by the pyrimidine, 5-fluorouracil (FU). It was shown previously that methanogenesis is not inhibited to the same extent as growth. A spontaneously occurring FU-resistant strain (RTAE-1) was isolated from a culture of strain Marburg. The growth of both strains was inhibited by 5-fluorodeoxyuridine but not 5-fluorocytosine, and the wild type was more susceptible to inhibition by 5-azauracil and 6-azauracil than was strain RTAE-1. The cellular targets for the pyrimidine analogs are not known. When the accumulation of 14C-labeled uracil or FU by the two strains was compared, the wild type took up 15-fold more radiolabel per cell than did the FU-resistant strain. In the wild type, radiolabel from uracil was incorporated into the soluble pool, RNA, and DNA. The metabolism of uracil appeared to involve a uracil phosphoribosyltransferase activity. Strain Marburg extracts contained this enzyme, whereas FU-resistant strain RTAE-1 extracts had less than 1/10 as much activity. Although it is possible that a change in permeability to the compounds plays a role in the stable resistance of strain RTAE-1, the fact that it lacks the ability to metabolize pyrimidines to nucleotides is sufficient to account for its phenotype. |
| Databáze: | OpenAIRE |
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