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Bacterial antibiotic resistance evolves through gene expression changes. We found that gene duplication, specifically of the folA gene, enhances dihydrofolate reductase (DHFR) levels, contributing to trimethoprim resistance in E. coli.

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Area of Science:

  • Microbiology
  • Evolutionary Biology
  • Genetics

Background:

  • Antibiotic resistance in bacteria is often driven by changes in gene expression.
  • Previous work showed mutations at the mgrB locus in Escherichia coli lead to dihydrofolate reductase (DHFR) overexpression under trimethoprim exposure.
  • The folA gene encodes DHFR.

Purpose of the Study:

  • To investigate how DHFR levels are further enhanced during bacterial adaptation to trimethoprim.
  • To explore the role of gene duplication and copy number evolution in antibiotic resistance.
  • To understand the interplay between antibiotic pressure, gene dosage, and proteostasis in bacterial evolution.

Main Methods:

  • Studied spontaneous genomic segment duplication encompassing the folA gene in Escherichia coli.
  • Compared duplication frequency in wild-type and lon-knockout strains under trimethoprim pressure.
  • Performed long-term evolution experiments to observe the dynamics of folA duplications and point mutations.
  • Investigated the impact of proteolysis on DHFR mutants and gene copy number evolution.

Main Results:

  • Spontaneous duplication of a genomic segment containing folA was observed, significantly increasing DHFR levels.
  • Duplication frequency was elevated in a lon-knockout strain, influencing early trimethoprim adaptation.
  • Under antibiotic pressure, folA duplications were initially reversed but became stable when coupled with resistance-conferring point mutations.
  • Some populations maintained folA duplication even with resistant DHFR mutants to compensate for low abundance.
  • Proteolysis of drug-resistant DHFR mutants exacerbated expression demand, favoring gene copy number evolution.

Conclusions:

  • Gene dosage evolution, specifically folA duplication, is influenced by expression demand generated by antibiotics.
  • Proteostasis, through the proteolysis of drug-resistant DHFR mutants, plays a novel role in determining copy number evolution in antibiotic-resistant bacteria.
  • This study proposes a new mechanism linking protein stability and gene copy number changes in bacterial adaptation.