Binding of HQNO to beef-heart sub-mitochondrial particles

Ark, G. van; Berden, J.A.

doi:10.1016/0005-2728(77)90014-7

Cited by 116 publications

(59 citation statements)

References 29 publications

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“…In addition to antimycin, several other compounds block electron flow through the bcl site; they include BAL [lO,ll], NoHOQnO [12,13], mucidin [ [8,9], suggested that oxygen radical generation at site 2 might be related to the mechanism of QH2 oxidation in center o of the Q cycle [19,20].…”

Section: Abbreviationsmentioning

confidence: 99%

Effect of electron transfer inhibitors on superoxide generation in the cytochrome bc₁ site of the mitochondrial respiratory chain

et al. 1983

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Antimycin, 2‐nonyl‐4‐hydroxyquinoline N‐oxide and funiculosin induce O·− 2 generation by submitochondrial particles oxidizing succinate, whereas KCN, mucidin, myxothiazol or 2,3‐dimercaptopropanol inhibit O·− 2 generation. Thenoyltrifluoroacetone does not induce superoxide production by itself but slightly stimulates the reaction initiated by antimycin. The results indicate that auto‐oxidation of unstable ubisemiquinone formed in centre o of the Q‐cycle generates most of the O·− 2 radicals in the cytochrome bc 1‐site of the mitochondrial respiratory chain.

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Section: Abbreviationsmentioning

confidence: 99%

Effect of electron transfer inhibitors on superoxide generation in the cytochrome bc₁ site of the mitochondrial respiratory chain

et al. 1983

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“…In contrast, cells grown on 15 glucose show a low level of endogenous respiration, which is not stimulated by glucose, probably because of catabolite repression, and is only slightly increased by galactose. We performed respiration tests also in the presence of a low concentration of antimycin A, which inhibits the h-cl complex of the respiratory chain [24]. to distinguish between the O2 level used via the respiratory chain and that involved in the antimycin-insensitive respiration.…”

Section: Preparution Of Mitochondria1 D N a And R N Amentioning

confidence: 99%

Mitochondrial Transcripts in Glucose‐Repressed Cells of Saccharomyces cerevisiae

Baldacci

Zennaro

1982

European Journal of Biochemistry

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We have compared mitochondrial transcripts from yeast Saccharomyces cerevisiae strain D273-10B grown in the presence of 2 % galactose (non-repressed cells) or IS "/, glucose (glucose-repressed cells).The ethidium-bromide-stained electrophoretic pattern of mitochondrial RNAs from glucose-repressed cells shows a clear decrease of tRNAs. In addition, some RNA bands appear to be specific for a single growth condition. To identify these RNA species we have performed hybridization experiments with 32P-labelled mitochondrial DNA from petite mutant cells. The mitochondrial repeat units of the mutants retained only one of the following genes: oxil, oxi2, oxi3, oli2, cob and o l d . Unchanged amounts of oxi2 and 01i2 transcripts and reduced concentrations of olil and oxil putative mRNAs are present in glucose-repressed cells. In the same growth condition we observe a decreased processing of a precursor RNA species from the split cob gene and reduced amounts of transcripts corresponding to the first, second and fifth intron of the split oxi3 gene. The oxi3 first and second introns, whose transcripts are the most variable, include long open reading frames in their nucleotide sequence, but at present it is not known whether the corresponding RNA species have a functional role. Our results show that their concentrations are related to the growth condition.The growth of yeast Saccharomyces cerevisiae in a medium containing a high concentration of glucose results in a very strong decrease of respiration [l]. Many enzymes involved in the respiratory catabolism of glucose are actually inactivated and their synthesis is absent or reduced to undetectable levels [2,3]. Morphological changes of yeast mitochondria related to the glucose-repressed growth condition have also been described [4]. The mitochondrial protein synthesis [ 5 ] and the level of mitochondrial RNA polymerase [6] are lowered; however, all the mitochondrially coded proteins are synthesized [7]. In addition, the acylatable form of mt-tRNAs"' is not detectable in resting repressed cells [8]. The release from glucose repression results in the increase of mtRNA polymerase concentration [6] and of mitochondrial protein synthesis [ S ] ; the respiratory catabolism of the carbon source is also restored [2].Glucose repression (and the release from it) in S. cerevisiue involves a coordinated expression of nuclear and mitochondrial genomes IS].In order to understand better the molecular events involved in this phenomenon, we compared the mitochondrial transcripts obtained from glucose-repressed cells with those observed in non-repressed conditions [lo]. The physiological meaning of the observed differences is also discussed. MATERIALS A N D METHODS Strains and Culrure ConditionsThe haploid strain D273-10B was grown aerobically at 28 "C in a medium containing 1 "/, yeast extract, 1 peptone and 2 % galactose or 15% glucose. Mid-exponential phase cells were harvested and used to prepare mtRNAs (see below).The rho-strains, kindly provided

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“…The specific mechanism for this activity remains unclear and is likely to be multifactorial, as anthraniloyl-CoA can serve as the precursor for at least 55 unique alkylquinolone (AQ) molecules (29,31). One of these, 2-heptyl-4-hydroxyquinoline N-oxide (HQNO), is an N-oxide ubiquinone that inhibits growth of Gram-positive bacteria, including S. aureus (32)(33)(34)(35)(36). Additionally, PQS stimulates the production of redox active phenazines, which may contribute to iron acquisition due to (i) their ability to lyse bacterial and mammalian cells (37), thus liberating intracellular iron stores, and (ii) redox cycling, which reduces insoluble ferric iron to its more bioavailable, ferrous form (38).…”

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Iron Depletion Enhances Production of Antimicrobials by Pseudomonas aeruginosa

et al. 2015

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Cystic fibrosis (CF) is a heritable disease characterized by chronic, polymicrobial lung infections. While Staphylococcus aureus is the dominant lung pathogen in young CF patients, Pseudomonas aeruginosa becomes predominant by adulthood. P. aeruginosa produces a variety of antimicrobials that likely contribute to this shift in microbial populations. In particular, secretion of 2-alkyl-4(1H)-quinolones (AQs) contributes to lysis of S. aureus in coculture, providing an iron source to P. aeruginosa both in vitro and in vivo. We previously showed that production of one such AQ, the Pseudomonas quinolone signal (PQS), is enhanced by iron depletion and that this induction is dependent upon the iron-responsive PrrF small RNAs (sRNAs). Here, we demonstrate that antimicrobial activity against S. aureus during coculture is also enhanced by iron depletion, and we provide evidence that multiple AQs contribute to this activity. Strikingly, a P. aeruginosa ⌬prrF mutant, which produces very little PQS in monoculture, was capable of mediating iron-regulated growth suppression of S. aureus. We show that the presence of S. aureus suppresses the ⌬prrF1,2 mutant's defect in iron-regulated PQS production, indicating that a PrrF-independent iron regulatory pathway mediates AQ production in coculture. We further demonstrate that iron-regulated antimicrobial production is conserved in multiple P. aeruginosa strains, including clinical isolates from CF patients. These results demonstrate that iron plays a central role in modulating interactions of P. aeruginosa with S. aureus. Moreover, our studies suggest that established iron regulatory pathways of these pathogens are significantly altered during polymicrobial infections. IMPORTANCEChronic polymicrobial infections involving Pseudomonas aeruginosa and Staphylococcus aureus are a significant cause of morbidity and mortality, as the interplay between these two organisms exacerbates infection. This is in part due to enhanced production of antimicrobial metabolites by P. aeruginosa when these two species are cocultured. Using both established and newly developed coculture techniques, this report demonstrates that iron depletion increases P. aeruginosa's ability to suppress growth of S. aureus. These findings present a novel role for iron in modulating microbial interaction and provide the basis for understanding how essential nutrients drive polymicrobial infections.

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Binding of HQNO to beef-heart sub-mitochondrial particles

Cited by 116 publications

References 29 publications

Effect of electron transfer inhibitors on superoxide generation in the cytochrome bc₁ site of the mitochondrial respiratory chain

Effect of electron transfer inhibitors on superoxide generation in the cytochrome bc₁ site of the mitochondrial respiratory chain

Mitochondrial Transcripts in Glucose‐Repressed Cells of Saccharomyces cerevisiae

Iron Depletion Enhances Production of Antimicrobials by Pseudomonas aeruginosa

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Binding of HQNO to beef-heart sub-mitochondrial particles

Cited by 116 publications

References 29 publications

Effect of electron transfer inhibitors on superoxide generation in the cytochrome bc1 site of the mitochondrial respiratory chain

Effect of electron transfer inhibitors on superoxide generation in the cytochrome bc1 site of the mitochondrial respiratory chain

Mitochondrial Transcripts in Glucose‐Repressed Cells of Saccharomyces cerevisiae

Iron Depletion Enhances Production of Antimicrobials by Pseudomonas aeruginosa

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Effect of electron transfer inhibitors on superoxide generation in the cytochrome bc₁ site of the mitochondrial respiratory chain

Effect of electron transfer inhibitors on superoxide generation in the cytochrome bc₁ site of the mitochondrial respiratory chain