ArticlePLoS pathogens2011
Compensatory evolution of pbp mutations restores the fitness cost imposed by β-lactam resistance in Streptococcus pneumoniae.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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43 citing papers in PubMed, 83 citations in OpenAlex.
- Genomic and statistical models to characterizeMicrobial genomics · 2026Article
- A mini review of genome-predicted β-lactam susceptibility inFrontiers in cellular and infection microbiology · 2026Review
- The effect of MurM and a branched cell wall structure on penicillin resistance inJournal of bacteriology · 2025Article
- Ceftolozane/tazobactam disrupts Pseudomonas aeruginosa biofilms under static and dynamic conditions.The Journal of antimicrobial chemotherapy · 2025Article
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- Coordinated regulation of osmotic imbalance by c-di-AMP shapes ß-lactam tolerance in Group BmicroLife · 2024Article
- Vaccination to Reduce Antimicrobial Resistance Burden-Data Gaps and Future Research.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2023Article
- Fructose promotes ampicillin killing of antibiotic-resistantVirulence · 2023Article
- Interspecies recombination, not de novo mutation, maintains virulence after β-lactam resistance acquisition in Streptococcus pneumoniae.Cell reports · 2022Article
- How Streptococcus suis escapes antibiotic treatments.Veterinary research · 2022Review
- Invasive Group A Streptococcal Penicillin Binding Protein 2× Variants Associated with Reduced Susceptibility to β-Lactam Antibiotics in the United States, 2015-2021.Antimicrobial agents and chemotherapy · 2022Article
- The acquisition of clinically relevant amoxicillin resistance in Streptococcus pneumoniae requires ordered horizontal gene transfer of four loci.PLoS pathogens · 2022Article
- Amoxicillin-resistanteLife · 2022Article
- Evolutionary Pathways and Trajectories in Antibiotic Resistance.Clinical microbiology reviews · 2021Article
- Large-scale genomic analysis of antimicrobial resistance in the zoonotic pathogen Streptococcus suis.BMC biology · 2021Article
- Article
- Population Genomic Molecular Epidemiological Study of Macrolide-Resistant Streptococcus pyogenes in Iceland, 1995 to 2016: Identification of a Large Clonal Population with aJournal of clinical microbiology · 2020Article
- The pneumococcal two-component system SirRH is linked to enhanced intracellular survival of Streptococcus pneumoniae in influenza-infected pulmonary cells.PLoS pathogens · 2020Article
- Broad-spectrum suppression of bacterial pneumonia by aminoglycoside-propagated Acinetobacter baumannii.PLoS pathogens · 2020Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prevalence of antibiotic resistance genes in pathogenic bacteria is a major challenge to treating many infectious diseases. The spread of these genes is driven by the strong selection imposed by the use of antibacterial drugs. However, in the absence of drug selection, antibiotic resistance genes impose a fitness cost, which can be ameliorated by compensatory mutations. In Streptococcus pneumoniae, β-lactam resistance is caused by mutations in three penicillin-binding proteins, PBP1a, PBP2x, and PBP2b, all of which are implicated in cell wall synthesis and the cell division cycle. We found that the fitness cost and cell division defects conferred by pbp2b mutations (as determined by fitness competitive assays in vitro and in vivo and fluorescence microscopy) were fully compensated by the acquisition of pbp2x and pbp1a mutations, apparently by means of an increased stability and a consequent mislocalization of these protein mutants. Thus, these compensatory combinations of pbp mutant alleles resulted in an increase in the level and spectrum of β-lactam resistance. This report describes a direct correlation between antibiotic resistance increase and fitness cost compensation, both caused by the same gene mutations acquired by horizontal transfer. The clinical origin of the pbp mutations suggests that this intergenic compensatory process is involved in the persistence of β-lactam resistance among circulating strains. We propose that this compensatory mechanism is relevant for β-lactam resistance evolution in Streptococcus pneumoniae.
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