ArticleInfection and immunity2003
Correlation of acetate catabolism and growth yield in Staphylococcus aureus: implications for host-pathogen interactions.
Article in Infection and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 141 citations in OpenAlex.
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- Unraveling proteomic chaos by independent component analysis-ClpX proficiency promotes the iron and oxygen limitation responses ofmSystems · 2025Article
- Growth and acetate metabolism ofApplied and environmental microbiology · 2025Article
- Pyrimidine sufficiency is required for Sae two-component system signaling inJournal of bacteriology · 2025Article
- Quaternized chitosan derivatives inhibit growth and affect biofilm formation of Staphylococcus aureus.Scientific reports · 2025Article
- Immune dysfunction during S. aureus biofilm-associated implant infections: opportunities for novel therapeutic strategies.NPJ biofilms and microbiomes · 2025Review
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- Core and accessory genomic traits of Vibrio cholerae O1 drive lineage transmission and disease severity.Nature communications · 2024Article
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- Altered quorum sensing and physiology of Staphylococcus aureus during spaceflight detected by multi-omics data analysis.NPJ microgravity · 2024Article
- Exploring the targetome of IsrR, an iron-regulated sRNA controlling the synthesis of iron-containing proteins inFrontiers in microbiology · 2024Article
- Elevated acetate kinase (ackA) gene expression, activity, and biofilm formation observed in methicillin-resistant strains of Staphylococcus aureus (MRSA).Journal, genetic engineering & biotechnology · 2023Article
- Horizontal Transfer of Bacteriocin Biosynthesis Genes Requires Metabolic Adaptation To Improve Compound Production and Cellular Fitness.Microbiology spectrum · 2023Article
- Role of sodium pyruvate in maintaining the survival and cytotoxicity ofFrontiers in microbiology · 2023Article
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- Thirty Years of sRNA-Mediated Regulation inInternational journal of molecular sciences · 2022Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, we reported that the prototypical Staphylococcus aureus strain RN6390 (a derivative of NCTC 8325) had significantly reduced aconitase activity relative to a diverse group of S. aureus isolates, leading to the hypothesis that strain RN6390 has impaired tricarboxylic acid (TCA) cycle-mediated acetate catabolism. Analysis of the culture supernatant from RN6390 confirmed that acetate was incompletely catabolized, suggesting that the ability to catabolize acetate can be lost by S. aureus. To test this hypothesis, we examined the carbon catabolism of the S. aureus strains whose genome sequences are publicly available. All strains catabolized glucose and excreted acetate into the culture medium. However, strains NCTC 8325 and N315 failed to catabolize acetate during the postexponential growth phase, resulting in significantly lower growth yields relative to strains that catabolized acetate. Strains NCTC 8325 and RN6390 contained an 11-bp deletion in rsbU, the gene encoding a positive regulator of the alternative sigma factor sigma(B) encoded by sigB. An isogenic derivative strain of RN6390 containing the wild-type rsbU gene had significantly increased acetate catabolism, demonstrating that sigma(B) is required for acetate catabolism. Taken together, the data suggest that naturally occurring mutations can alter the ability of S. aureus to catabolize acetate, a surprising discovery, as TCA cycle function has been demonstrated to be involved in the virulence, survival, and persistence of several pathogenic organisms. Additionally, these mutations decrease the fitness of S. aureus by reducing the number of progeny placed into subsequent generations, suggesting that in certain situations a decreased growth yield is advantageous.
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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.