ArticleJournal of bacteriology2012
Decreased transport restores growth of a Salmonella enterica apbC mutant on tricarballylate.
Article in Journal of bacteriology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed.
- Regulation of tricarboxylate transport and metabolism inApplied and environmental microbiology · 2024Article
- Cetylpyridinium Trichlorostannate: Synthesis, Antimicrobial Properties, and Controlled-Release Properties via Electrical Resistance Tomography.ACS omega · 2021Article
- Review
- Genetic Approaches to Uncover Gene Products Involved in Iron-Sulfur Protein Maturation: High-Throughput Genomic Screening Using Transposon Sequencing.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Synthesis, Characterization, and Antimicrobial Investigation of a Novel Chlorhexidine Cyclamate Complex.Crystal growth & design · 2020Article
- Synthesis, Characterization, and Investigation of the Antimicrobial Activity of Cetylpyridinium Tetrachlorozincate.ACS omega · 2020Article
- The bacterial MrpScientific reports · 2019Article
- Lactobacillus paracasei metabolism of rice bran reveals metabolome associated with Salmonella Typhimurium growth reduction.Journal of applied microbiology · 2017Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Mutants of Salmonella enterica lacking apbC have nutritional and biochemical properties indicative of defects in iron-sulfur ([Fe-S]) cluster metabolism. An apbC mutant is unable to grow on tricarballylate as a carbon source. Based on the ability of ApbC to transfer an [Fe-S] cluster to an apoprotein, this defect was attributed to poor loading of the [Fe-S] cluster-containing TcuB enzyme. Consistent with these observations, a previous study showed that overexpression of iscU, which encodes an [Fe-S] cluster molecular scaffold, suppressed the tricarballylate growth defect of an apbC mutant (J. M. Boyd, J. A. Lewis, J. C. Escalante-Semerena, and D. M. Downs, J. Bacteriol. 190:4596-4602, 2008). In this study, tcuC mutations that suppress the growth defect of an apbC mutant by decreasing the intracellular concentration of tricarballylate are described. Collectively, the suppressor analyses support a model in which reduced TcuB activity prevents growth on tricarballylate by (i) decreasing catabolism and (ii) allowing levels of tricarballylate that are toxic to the cell to accumulate. The apbC tcuC mutant strains described here reveal that the balance of the metabolic network can be altered by the accumulation of deleterious metabolites.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.