ArticleJournal of bacteriology2014
Deoxycytidine deaminase-deficient Escherichia coli strains display acute sensitivity to cytidine, adenosine, and guanosine and increased sensitivity to a range of antibiotics, including vancomycin.
Article in Journal of bacteriology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Bioinformatic Analysis of Sulfotransferases from an Unexplored Gut Microbe,International journal of molecular sciences · 2024Article
- Oxidation of dCTP contributes to antibiotic lethality in stationary-phase mycobacteria.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Mutagen Synergy: Hypermutability Generated by Specific Pairs of Base Analogs.Journal of bacteriology · 2016Article
- Synergistic interactions of vancomycin with different antibiotics against Escherichia coli: trimethoprim and nitrofurantoin display strong synergies with vancomycin against wild-type E. coli.Antimicrobial agents and chemotherapy · 2015Article
- Extreme dNTP pool changes and hypermutability in dcd ndk strains.Mutation researchArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We show here that deoxycytidine deaminase (DCD)-deficient mutants of Escherichia coli are hypersensitive to killing by exogenous cytidine, adenosine, or guanosine, whereas wild-type cells are not. This hypersensitivity is reversed by exogenous thymidine. The mechanism likely involves the allosteric regulation of ribonucleotide reductase and severe limitations of the dTTP pools, resulting in thymineless death, the phenomenon of cell death due to thymidine starvation. We also report here that DCD-deficient mutants of E. coli are more sensitive to a series of different antibiotics, including vancomycin, and we show synergistic killing with the combination of vancomycin and cytidine. One possibility is that a very low, subinhibitory concentration of vancomycin enters Gram-negative cells and that this concentration is potentiated by chromosomal lesions resulting from the thymineless state. A second possibility is that the metabolic imbalance resulting from DCD deficiency affects the assembly of the outer membrane, which normally presents a barrier to drugs such as vancomycin. We consider these findings with regard to ideas of rendering Gram-negative bacteria sensitive to drugs such as vancomycin.
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Registered trials
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