ArticleGenetics2009
The fitness cost of streptomycin resistance depends on rpsL mutation, carbon source and RpoS (sigmaS).
Article in Genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 112 citations in OpenAlex.
- Host oxidative stress primes mycobacteria for rapid antibiotic resistance evolution.Nature communications · 2026Article
- Loss of DNA mismatch repair genes leads to acquisition of antibiotic resistance independent of secondary mutations.PLoS genetics · 2026Article
- Antibiotic resistance increases evolvability and maximizes opportunities across fitness landscapes.Frontiers in microbiology · 2026Article
- Host oxidative stress primes mycobacteria for rapid antibiotic resistance evolution.Research square · 2025Article
- Idiosyncratic evolvability among single-point ribosomal mutants towards multi-aminoglycoside resistance.PLoS genetics · 2025Article
- Carvacrol and Streptomycin in Combination Weaken Streptomycin Resistance inPlants (Basel, Switzerland) · 2025Article
- What Is the Impact of Antibiotic Resistance Determinants on the Bacterial Death Rate?Antibiotics (Basel, Switzerland) · 2025Article
- An eco-evolutionary perspective on antimicrobial resistance in the context of One Health.iScience · 2025Review
- Costs of antibiotic resistance genes depend on host strain and environment and can influence community composition.Proceedings. Biological sciences · 2024Article
- Antibiotic resistance begets more resistance: chromosomal resistance mutations mitigate fitness costs conferred by multi-resistant clinical plasmids.Microbiology spectrum · 2024Article
- Convergent genetic adaptation ofFrontiers in molecular biosciences · 2024Article
- Cultivating antimicrobial resistance: how intensive agriculture ploughs the way for antibiotic resistance.Microbiology (Reading, England) · 2023Review
- Heterogeneity among Clinical Intestinal Escherichia coli Isolates upon Acquired Streptomycin Resistance.Microbiology spectrum · 2023Article
- Case Studies in the Assessment of Microbial Fitness: Seemingly Subtle Changes Can Have Major Effects on Phenotypic Outcomes.Journal of molecular evolution · 2023Article
- Survey of Oxolinic Acid-Resistant Erwinia amylovora in Korean Apple and Pear Orchards, and the Fitness Impact of Constructed Mutants.The plant pathology journal · 2022Article
- Bacterial Stress Responses as Potential Targets in Overcoming Antibiotic Resistance.Microorganisms · 2022Review
- Antibiotic Minimal Selective Concentrations and Fitness Costs during Biofilm and Planktonic Growth.mBio · 2022Article
- Nutrient Limitation Magnifies Fitness Costs of Antimalarial Drug Resistance Mutations.Antimicrobial agents and chemotherapy · 2022Article
- Physiological Responses of Ribosomal Protein S12 K43 Mutants of Corynebacterium glutamicum.Current microbiology · 2022Article
- Translational demand is not a major source of plasmid-associated fitness costs.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations that cause antibiotic resistance often produce associated fitness costs. These costs have a detrimental effect on the fate of resistant organisms in natural populations and could be exploited in designing drugs, therapeutic regimes, and intervention strategies. The streptomycin resistance (StrR) mutations K42N and P90S in ribosomal protein S12 impair growth on rich medium. Surprisingly, in media with poorer carbon sources, the same StrR mutants grow faster than wild type. This improvement reflects a failure of these StrR mutants to induce the stress-inducible sigma factor RpoS (sigmaS), a key regulator of many stationary-phase and stress-inducible genes. On poorer carbon sources, wild-type cells induce sigmaS, which retards growth. By not inducing sigmaS, StrR mutants escape this self-imposed inhibition. Consistent with this interpretation, the StrR mutant loses its advantage over wild type when both strains lack an RpoS (sigmaS) gene. Failure to induce sigmaS produced the following side effects: (1) impaired induction of several stress-inducible genes, (2) reduced tolerance to thermal stress, and (3) reduced translational fidelity. These results suggest that RpoS may contribute to long-term cell survival, while actually limiting short-term growth rate under restrictive growth conditions. Accordingly, the StrR mutant avoids short-term growth limitation but is sensitized to other stresses. These results highlight the importance of measuring fitness costs under multiple experimental conditions not only to acquire a more relevant estimate of fitness, but also to reveal novel physiological weaknesses exploitable for drug development.
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Registered trials
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.