ArticleMolecular microbiology2011
Fructose-1,6-bisphosphate aldolase (class II) is the primary site of nickel toxicity in Escherichia coli.
Article in Molecular microbiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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
28 citing papers in PubMed, 73 citations in OpenAlex.
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- Assignment of the antibacterial potential of AgBrazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2023Article
- Conversion ofMicroorganisms · 2023Article
- Soft-metal(loid)s induce protein aggregation inFrontiers in microbiology · 2023Article
- Combination Strategies of Different Antimicrobials: An Efficient and Alternative Tool for Pathogen Inactivation.Biomedicines · 2022Review
- Coordination Properties of the Zinc Domains of BigR4 and SmtB Proteins in Nickel Systems─Designation of Key Donors.Inorganic chemistry · 2022Article
- Loss of Mobile Genomic Islands in Metal-Resistant, Hydrogen-Oxidizing Cupriavidus metallidurans.Applied and environmental microbiology · 2022Article
- Protein metalation in biology.Current opinion in chemical biology · 2022Review
- Ynt is the primary nickel import system used by Proteus mirabilis and specifically contributes to fitness by supplying nickel for urease activity.Molecular microbiology · 2020Article
- Response of particle-associated bacteria to long-term heavy metal contamination in a tropical estuary.World journal of microbiology & biotechnology · 2020Article
- Silver-coated magnetic nanocomposites induce growth inhibition and protein changes in foodborne bacteria.Scientific reports · 2019Article
- Article
- Metalloproteins in the Biology of Heterocysts.Life (Basel, Switzerland) · 2019Review
- Nickel exposure reduces enterobactin production in Escherichia coli.MicrobiologyOpen · 2019Article
- Uropathogenic enterobacteria use the yersiniabactin metallophore system to acquire nickel.The Journal of biological chemistry · 2018Article
- Metalloriboswitches: RNA-based inorganic ion sensors that regulate genes.The Journal of biological chemistry · 2017Review
- Functional Determinants of Metal Ion Transport and Selectivity in Paralogous Cation Diffusion Facilitator Transporters CzcD and MntE in Streptococcus pneumoniae.Journal of bacteriology · 2016Article
- The Escherichia coli small protein MntS and exporter MntP optimize the intracellular concentration of manganese.PLoS genetics · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Nickel is toxic to all forms of life, but the mechanisms of cell damage are unknown. Indeed, environmentally relevant nickel levels (8 µM) inhibit wild-type Escherichia coli growth on glucose minimal medium. The same concentration of nickel also inhibits growth on fructose, but not succinate, lactate or glycerol; these results suggest that fructose-1,6-bisphosphate aldolase (FbaA) is a target of nickel toxicity. Cells stressed by 8 µM Ni(II) for 20 min lost 75% of their FbaA activity, demonstrating that FbaA is inactivated during nickel stress. Furthermore, overexpression of fbaA restored growth of an rcnA mutant in glucose minimal medium supplemented with 4 µM Ni(II), thus confirming that FbaA is a primary target of nickel toxicity. This class II aldolase has an active site zinc and a non-catalytic zinc nearby. Purified FbaA lost 80 % of its activity within 2 min when challenged with 8 µM Ni(II). Nickel-challenged FbaA lost 0.8 zinc and gained 0.8 nickel per inactivated monomer. FbaA mutants (D144A and E174A) affecting the non-catalytic zinc were resistant to nickel inhibition. These results define the primary site of nickel toxicity in E. coli as the class II aldolase FbaA through binding to the non-catalytic zinc site.
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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.