PMID:2191080
| Citation |
Birch, RG, Pemberton, JM and Basnayake, WV (1990) Stable albicidin resistance in Escherichia coli involves an altered outer-membrane nucleoside uptake system.J. Gen. Microbiol. 136:51-8 |
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| Abstract |
Albicidin blocked DNA synthesis in intact cells of a PolA- EndA- Escherichia coli strain, and in permeabilized cells supplied with all necessary precursor nucleotides, indicating a direct effect on prokaryote DNA replication. Replication of phages T4 and T7 was also blocked by albicidin in albicidin-sensitive (Albs) but not in albicidin-resistant (Albr) E. coli host-cells. All stable spontaneous Albr mutants of E. coli simultaneously became resistant to phage T6. The locus determining albicidin sensitivity mapped at tsx, the structural gene for an outer-membrane protein used as a receptor by phage T6 and involved in transport through the outer membrane of nucleosides present at submicromolar extracellular concentrations. Albicidin does not closely resemble a nucleoside in structure. However, Albs E. coli strains rapidly accumulated both nucleosides and albicidin from the surrounding medium whereas the Albr mutants were defective in uptake of nucleosides and albicidin at low extracellular concentrations. An insertion mutation blocking Tsx protein production also blocked albicidin uptake and conveyed albicidin resistance. Albicidin supplied at approximately 0.1 microM blocked DNA replication within seconds in intact Albs E. coli cells, but a 100-fold higher albicidin concentration was necessary for a rapid inhibition of DNA replication in permeabilized cells. We conclude that albicidin is effective at very low concentrations against E. coli because it is rapidly concentrated within cells by illicit transport through the tsx-encoded outer-membrane channel normally involved in nucleoside uptake. Albicidin resistance results from loss of the mechanism of albicidin transport through the outer membrane. |
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| Keywords |
Anti-Bacterial Agents; Cell Membrane; Chromosome Mapping; Dose-Response Relationship, Drug; Drug Resistance, Microbial; Escherichia coli; Mutation; Nucleosides; Organic Chemicals; Xanthomonas |
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Main Points of the Paper
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Materials and Methods Used
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Phenotype Annotations
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| Phenotype of | Taxon Information | Genotype Information (if known) | Condition Information | OMP ID | OMP Term Name | ECO ID | ECO Term Name | Notes | Status |
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a mutation or genetic difference within a strain |
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0000276 |
increased resistance to antibiotics |
0000181 |
in vitro assay evidence |
mutation to the tsx region greatly reduced sensitivity toward albicidin. See Figure 1 B for full experimental results. |
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a mutation or genetic difference within a strain |
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0000252 |
metabolite accumulation |
0000181 |
in vitro assay evidence |
mutation to the tsx region which causes a reduction in nucleoside uptake. See figure 2 for full experimental results. |
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a mutation or genetic difference within a strain |
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0000252 |
metabolite accumulation |
0000181 |
in vitro assay evidence |
mutation to the tsx region which caused its suppression showed that there was a reduction albicidin uptake, indicating that alicidin resistance is due to the reduction in its uptake. See figure 3b for full results. Figure 3a shows similar data with strains Q358 and Q358 Albr. |
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Notes
- the alb locus was mapped close to the tsx gene. See table 2 for Pl transduction experiment results.
References
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