ArticleThe Journal of biological chemistry2015
A novel A3 group aconitase tolerates oxidation and nitric oxide.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 13 citations in OpenAlex.
- Metabolic plasticity enables Clostridioides difficile growth in coculture with neutrophils and other mammalian cells.Anaerobe · 2025Article
- The Metabolic Regulation of Amino Acid Synthesis Counteracts Reactive Nitrogen Stress viaJournal of fungi (Basel, Switzerland) · 2024Article
- Article
- Functional characterization of aconitase X as a cis-3-hydroxy-L-proline dehydratase.Scientific reports · 2016Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Achromobacter denitrificans YD35 is an NO2 (-)-tolerant bacterium that expresses the aconitase genes acnA3, acnA4, and acnB, of which acnA3 is essential for growth tolerance against 100 mm NO2 (-). Atmospheric oxygen inactivated AcnA3 at a rate of 1.6 × 10(-3) min(-1), which was 2.7- and 37-fold lower compared with AcnA4 and AcnB, respectively. Stoichiometric titration showed that the [4Fe-4S](2+) cluster of AcnA3 was more stable against oxidative inactivation by ferricyanide than that of AcnA4. Aconitase activity of AcnA3 persisted against high NO2 (-) levels that generate reactive nitrogen species with an inactivation rate constant of k = 7.8 × 10(-3) min(-1), which was 1.6- and 7.8-fold lower than those for AcnA4 and AcnB, respectively. When exposed to NO2 (-), the acnA3 mutant (AcnA3Tn) accumulated higher levels of cellular citrate compared with the other aconitase mutants, indicating that AcnA3 is a major producer of cellular aconitase activity. The extreme resistance of AcnA3 against oxidation and reactive nitrogen species apparently contributes to bacterial NO2 (-) tolerance. AcnA3Tn accumulated less cellular NADH and ATP compared with YD35 under our culture conditions. The accumulation of more NO by AcnA3Tn suggested that NADH-dependent enzymes detoxify NO for survival in a high NO2 (-) milieu. This novel aconitase is distributed in Alcaligenaceae bacteria, including pathogens and denitrifiers, and it appears to contribute to a novel NO2 (-) tolerance mechanism in this strain.
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