ArticleThe Journal of biological chemistry2011
Loss of a conserved tyrosine residue of cytochrome b induces reactive oxygen species production by cytochrome bc1.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 41 citations in OpenAlex.
- Catalytic Reactions and Energy Conservation in the CytochromeChemical reviews · 2021Review
- Mitochondrial UQCRC1 mutations cause autosomal dominant parkinsonism with polyneuropathy.Brain : a journal of neurology · 2020Article
- The anti-malarial drug atovaquone potentiates platinum-mediated cancer cell death by increasing oxidative stress.Cell death discovery · 2020Article
- Minimization of energy transduction confers resistance to phosphine in the rice weevil, Sitophilus oryzae.Scientific reports · 2019Article
- Bifidobacteria and the infant gut: an example of co-evolution and natural selection.Cellular and molecular life sciences : CMLS · 2018Review
- Mitochondrial disease-related mutations at the cytochrome b-iron-sulfur protein (ISP) interface: Molecular effects on the large-scale motion of ISP and superoxide generation studied in Rhodobacter capsulatus cytochrome bc1.Biochimica et biophysica acta · 2016Article
- Saccharomyces cerevisiae-based mutational analysis of the bc1 complex Qo site residue 279 to study the trade-off between atovaquone resistance and function.Antimicrobial agents and chemotherapy · 2015Article
- Mitochondrial DNA association study of type 2 diabetes with or without ischemic stroke in Taiwan.BMC research notes · 2014Article
- Structural basis of resistance to anti-cytochrome bc₁ complex inhibitors: implication for drug improvement.Current pharmaceutical design · 2014Review
- The cytochrome b p.278Y>C mutation causative of a multisystem disorder enhances superoxide production and alters supramolecular interactions of respiratory chain complexes.Human molecular genetics · 2013Article
- Role of the -PEWY-glutamate in catalysis at the Q(o)-site of the Cyt bc(1) complex.Biochimica et biophysica acta · 2013Article
- Reconstructing the Qo site of Plasmodium falciparum bc 1 complex in the yeast enzyme.PloS one · 2013Article
- Generation, characterization and crystallization of a cytochrome c(1)-subunit IV fused cytochrome bc(1) complex from Rhodobacter sphaeroides.Biochimica et biophysica acta · 2012Article
- Molecular mechanisms of superoxide production by complex III: a bacterial versus human mitochondrial comparative case study.Biochimica et biophysica actaReview
- The mechanism of ubihydroquinone oxidation at the Qo-site of the cytochrome bc1 complex.Biochimica et biophysica actaReview
- Structural analysis of cytochrome bc1 complexes: implications to the mechanism of function.Biochimica et biophysica actaReview
- Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Production of reactive oxygen species (ROS) induces oxidative damages, decreases cellular energy conversion efficiencies, and induces metabolic diseases in humans. During respiration, cytochrome bc(1) efficiently oxidizes hydroquinone to quinone, but how it performs this reaction without any leak of electrons to O(2) to yield ROS is not understood. Using the bacterial enzyme, here we show that a conserved Tyr residue of the cytochrome b subunit of cytochrome bc(1) is critical for this process. Substitution of this residue with other amino acids decreases cytochrome bc(1) activity and enhances ROS production. Moreover, the Tyr to Cys mutation cross-links together the cytochrome b and iron-sulfur subunits and renders the bacterial enzyme sensitive to O(2) by oxidative disruption of its catalytic [2Fe-2S] cluster. Hence, this Tyr residue is essential in controlling unproductive encounters between O(2) and catalytic intermediates at the quinol oxidation site of cytochrome bc(1) to prevent ROS generation. Remarkably, the same Tyr to Cys mutation is encountered in humans with mitochondrial disorders and in Plasmodium species that are resistant to the anti-malarial drug atovaquone. These findings illustrate the harmful consequences of this mutation in human diseases.
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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.