Copper ions inhibit pentose phosphate pathway function in Staphylococcus aureus.

To gain a better insight of how Copper (Cu) ions toxify cells, metabolomic analyses were performed in S. aureus strains that lacks the described Cu ion detoxification systems (ΔcopBL ΔcopAZ; cop-). Exposure of the cop- strain to Cu(II) resulted in an increase in the concentrations of metabolites uti...

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Main Authors: Javiera Norambuena, Hassan Al-Tameemi, Hannah Bovermann, Jisun Kim, William N Beavers, Eric P Skaar, Dane Parker, Jeffrey M Boyd
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2023-05-01
Series:PLoS Pathogens
Online Access:https://doi.org/10.1371/journal.ppat.1011393
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author Javiera Norambuena
Hassan Al-Tameemi
Hannah Bovermann
Jisun Kim
William N Beavers
Eric P Skaar
Dane Parker
Jeffrey M Boyd
author_facet Javiera Norambuena
Hassan Al-Tameemi
Hannah Bovermann
Jisun Kim
William N Beavers
Eric P Skaar
Dane Parker
Jeffrey M Boyd
author_sort Javiera Norambuena
collection DOAJ
description To gain a better insight of how Copper (Cu) ions toxify cells, metabolomic analyses were performed in S. aureus strains that lacks the described Cu ion detoxification systems (ΔcopBL ΔcopAZ; cop-). Exposure of the cop- strain to Cu(II) resulted in an increase in the concentrations of metabolites utilized to synthesize phosphoribosyl diphosphate (PRPP). PRPP is created using the enzyme phosphoribosylpyrophosphate synthetase (Prs) which catalyzes the interconversion of ATP and ribose 5-phosphate to PRPP and AMP. Supplementing growth medium with metabolites requiring PRPP for synthesis improved growth in the presence of Cu(II). A suppressor screen revealed that a strain with a lesion in the gene coding adenine phosphoribosyltransferase (apt) was more resistant to Cu. Apt catalyzes the conversion of adenine with PRPP to AMP. The apt mutant had an increased pool of adenine suggesting that the PRPP pool was being redirected. Over-production of apt, or alternate enzymes that utilize PRPP, increased sensitivity to Cu(II). Increasing or decreasing expression of prs resulted in decreased and increased sensitivity to growth in the presence of Cu(II), respectively. We demonstrate that Prs is inhibited by Cu ions in vivo and in vitro and that treatment of cells with Cu(II) results in decreased PRPP levels. Lastly, we establish that S. aureus that lacks the ability to remove Cu ions from the cytosol is defective in colonizing the airway in a murine model of acute pneumonia, as well as the skin. The data presented are consistent with a model wherein Cu ions inhibits pentose phosphate pathway function and are used by the immune system to prevent S. aureus infections.
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spelling doaj-art-3f1de80caeeb4e4e89cb47459d3ed5dc2025-08-20T01:48:29ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742023-05-01195e101139310.1371/journal.ppat.1011393Copper ions inhibit pentose phosphate pathway function in Staphylococcus aureus.Javiera NorambuenaHassan Al-TameemiHannah BovermannJisun KimWilliam N BeaversEric P SkaarDane ParkerJeffrey M BoydTo gain a better insight of how Copper (Cu) ions toxify cells, metabolomic analyses were performed in S. aureus strains that lacks the described Cu ion detoxification systems (ΔcopBL ΔcopAZ; cop-). Exposure of the cop- strain to Cu(II) resulted in an increase in the concentrations of metabolites utilized to synthesize phosphoribosyl diphosphate (PRPP). PRPP is created using the enzyme phosphoribosylpyrophosphate synthetase (Prs) which catalyzes the interconversion of ATP and ribose 5-phosphate to PRPP and AMP. Supplementing growth medium with metabolites requiring PRPP for synthesis improved growth in the presence of Cu(II). A suppressor screen revealed that a strain with a lesion in the gene coding adenine phosphoribosyltransferase (apt) was more resistant to Cu. Apt catalyzes the conversion of adenine with PRPP to AMP. The apt mutant had an increased pool of adenine suggesting that the PRPP pool was being redirected. Over-production of apt, or alternate enzymes that utilize PRPP, increased sensitivity to Cu(II). Increasing or decreasing expression of prs resulted in decreased and increased sensitivity to growth in the presence of Cu(II), respectively. We demonstrate that Prs is inhibited by Cu ions in vivo and in vitro and that treatment of cells with Cu(II) results in decreased PRPP levels. Lastly, we establish that S. aureus that lacks the ability to remove Cu ions from the cytosol is defective in colonizing the airway in a murine model of acute pneumonia, as well as the skin. The data presented are consistent with a model wherein Cu ions inhibits pentose phosphate pathway function and are used by the immune system to prevent S. aureus infections.https://doi.org/10.1371/journal.ppat.1011393
spellingShingle Javiera Norambuena
Hassan Al-Tameemi
Hannah Bovermann
Jisun Kim
William N Beavers
Eric P Skaar
Dane Parker
Jeffrey M Boyd
Copper ions inhibit pentose phosphate pathway function in Staphylococcus aureus.
PLoS Pathogens
title Copper ions inhibit pentose phosphate pathway function in Staphylococcus aureus.
title_full Copper ions inhibit pentose phosphate pathway function in Staphylococcus aureus.
title_fullStr Copper ions inhibit pentose phosphate pathway function in Staphylococcus aureus.
title_full_unstemmed Copper ions inhibit pentose phosphate pathway function in Staphylococcus aureus.
title_short Copper ions inhibit pentose phosphate pathway function in Staphylococcus aureus.
title_sort copper ions inhibit pentose phosphate pathway function in staphylococcus aureus
url https://doi.org/10.1371/journal.ppat.1011393
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