In the respiratory chain of Escherichia coli cytochromes bd-I and bd-II are more sensitive to carbon monoxide inhibition than cytochrome bo3

Forte, Elena; Borisov, Vitaliy B.; Siletsky, Sergey A.; Petrosino, Maria; Giuffrè, Alessandro

doi:10.1016/j.bbabio.2019.148088

Cited by 26 publications

(18 citation statements)

References 80 publications

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“…In general, it resulted in the down-regulation of genes involved in the citric acid cycle and respiration (cyoABCDE and sdhABCD operon). However, small induction of the cydAB genes encoding cytochrome bd-I was observed, which is consistent with cytochrome bd-I being the more CO resistant oxidase [117]. Up-regulated genes were those participating in SOS response, DNA repair, protein homeostasis, zinc, methionine, sulfur and cysteine metabolism, and biofilm formation [85,116].…”

Section: Bacterial Responses To Toxic Cosupporting

confidence: 66%

Hydrogen Sulfide and Carbon Monoxide Tolerance in Bacteria

2021

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Hydrogen sulfide and carbon monoxide share the ability to be beneficial or harmful molecules depending on the concentrations to which organisms are exposed. Interestingly, humans and some bacteria produce small amounts of these compounds. Since several publications have summarized the recent knowledge of its effects in humans, here we have chosen to focus on the role of H2S and CO on microbial physiology. We briefly review the current knowledge on how bacteria produce and use H2S and CO. We address their potential antimicrobial properties when used at higher concentrations, and describe how microbial systems detect and survive toxic levels of H2S and CO. Finally, we highlight their antimicrobial properties against human pathogens when endogenously produced by the host and when released by external chemical donors.

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Section: Bacterial Responses To Toxic Cosupporting

confidence: 66%

Hydrogen Sulfide and Carbon Monoxide Tolerance in Bacteria

2021

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“…The resistance of cytochrome bd oxidase to CO in M. smegmatis is consistent with a previous report that an E. coli mutant possessing only cytochrome bd-I oxidase is resistant to inhibition by the CO-producing molecule CORM-3 ( 26 ). However, a recent study demonstrated that purified cytochrome bd-I and bd-II oxidases from E. coli are more sensitive to inhibition by gaseous CO than cytochrome bo′ oxidase ( 49 ). The difference between these findings may result from the use of CORM-3 for CO delivery in the former study.…”

Section: Discussionmentioning

confidence: 99%

Mycobacteria Tolerate Carbon Monoxide by Remodeling Their Respiratory Chain

et al. 2021

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Carbon monoxide (CO) gas is infamous for its acute toxicity. This toxicity predominantly stems from its tendency to form carbonyl complexes with transition metals, thus inhibiting the heme-prosthetic groups of proteins, including respiratory terminal oxidases. While CO has been proposed as an antibacterial agent, the evidence supporting its toxicity toward bacteria is equivocal, and its cellular targets remain poorly defined. In this work, we investigate the physiological response of mycobacteria to CO. We show that Mycobacterium smegmatis is highly resistant to the toxic effects of CO, exhibiting only minor inhibition of growth when cultured in its presence. We profiled the proteome of M. smegmatis during growth in CO, identifying strong induction of cytochrome bd oxidase and members of the dos regulon, but relatively few other changes. We show that the activity of cytochrome bd oxidase is resistant to CO, whereas cytochrome bcc-aa3 oxidase is strongly inhibited by this gas. Consistent with these findings, growth analysis shows that M. smegmatis lacking cytochrome bd oxidase displays a significant growth defect in the presence of CO, while induction of the dos regulon appears to be unimportant for adaptation to CO. Altogether, our findings indicate that M. smegmatis has considerable resistance to CO and benefits from respiratory flexibility to withstand its inhibitory effects. IMPORTANCE Carbon monoxide has an infamous reputation as a toxic gas, and it has been suggested that it has potential as an antibacterial agent. Despite this, how bacteria resist its toxic effects is not well understood. In this study, we investigated how CO influences growth, proteome, and aerobic respiration of wild-type and mutant strains of Mycobacterium smegmatis. We show that this bacterium produces the CO-resistant cytochrome bd oxidase to tolerate poisoning of its CO-sensitive complex IV homolog. Further, we show that aside from this remodeling of its respiratory chain, M. smegmatis makes few other functional changes to its proteome, suggesting it has a high level of inherent resistance to CO.

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“…The resistance of cytochrome bd oxidase to CO in M. smegmatis is consistent with a previous report showing that, in E. coli , a mutant possessing only cytochrome bd-I oxidase is less sensitive to growth inhibition by the CO producing molecule CORM-3 than mutants possessing only the other terminal oxidases (cytochrome bd-II and cytochrome bo’ ) of E. coli (44). However, a recent study demonstrated that purified cytochrome bd-I and bd-II oxidases from E. coli are more sensitive to inhibition by gaseous CO than cytochrome bo’ oxidase (45). The difference between these findings may result from the use of CORM-3 for CO delivery in the former study.…”

Section: Discussionmentioning

confidence: 99%

Mycobacteria tolerate carbon monoxide by remodelling their respiratory chain

Bayly

Cordero

Schittenhelm

et al. 2020

Preprint

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18Carbon monoxide (CO) is a gas infamous for its acute toxicity. The toxicity of CO 19 predominantly stems from its tendency to form carbonyl complexes with transition 20 metals, thus inhibiting the heme-prosthetic groups of proteins, including the terminal 21 oxidases of the respiratory chain. While CO has been proposed as an antibacterial 22 agent, the evidence supporting its toxicity towards bacteria is equivocal, and its 23 cellular targets remain poorly defined. In this work, we investigate the physiological 24 response of mycobacteria to CO. We show that Mycobacterium smegmatis is highly 25 resistant to the toxic effects of CO, exhibiting normal growth parameters when 26 cultured in its presence. We profiled the proteome of M. smegmatis during growth in 27 CO, identifying strong induction of cytochrome bd oxidase and members of the dos 28 regulon, but relatively few other changes. We show that the activity of cytochrome bd 29 oxidase is resistant to CO, whereas cytochrome bcc-aa 3 oxidase is strongly inhibited 30 by this gas. Consistent with these findings, growth analysis shows that M. smegmatis 31 lacking cytochrome bd oxidase displays a significant growth defect in the presence 32 of CO, while induction of the dos regulon appears to be unimportant for adaption to 33 CO. Altogether, our findings suggest that M. smegmatis has considerable resistance 34 to CO and benefits from respiratory flexibility to withstand its inhibitory effects. 35 36 Importance 37 Carbon monoxide has an infamous reputation as a toxic gas and it has been 38 suggested that it has potential as an antibacterial agent. Despite this, the means by 39 which bacteria resist its toxic effects are not well understood. In this study we 40 determine the physiological response of Mycobacterium smegmatis to growth in CO. 41 We show for the first time that the cytochrome bd oxidase is inherently resistant to 42 CO and is deployed by M. smegmatis to tolerate the presence of this gas. Further, 43we show that aside from this remodelling of its respiratory chain, M. smegmatis 44 makes few other functional changes to its proteome, suggesting it has a high level of 45 inherent resistance to CO. 46 47

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In the respiratory chain of Escherichia coli cytochromes bd-I and bd-II are more sensitive to carbon monoxide inhibition than cytochrome bo3

Cited by 26 publications

References 80 publications

Hydrogen Sulfide and Carbon Monoxide Tolerance in Bacteria

Hydrogen Sulfide and Carbon Monoxide Tolerance in Bacteria

Mycobacteria Tolerate Carbon Monoxide by Remodeling Their Respiratory Chain

Mycobacteria tolerate carbon monoxide by remodelling their respiratory chain

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