Whole-population genomic sequencing reveals the mutational profiles of the antibiotic-treated Escherichia coli populations


KÜÇÜKYILDIRIM ÇELİK S.

BIOLOGIA, vol.77, pp.525-531, 2022 (SCI-Expanded, Scopus) identifier identifier

  • Publication Type: Article / Article
  • Volume: 77
  • Publication Date: 2022
  • Doi Number: 10.1007/s11756-021-00959-8
  • Journal Name: BIOLOGIA
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, Agricultural & Environmental Science Database, Animal Behavior Abstracts, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, CAB Abstracts, Veterinary Science Database
  • Page Numbers: pp.525-531
  • Keywords: Antibiotic resistance, Mutation spectrum, Colistin, Quinolones, FLUOROQUINOLONE RESISTANCE, KLEBSIELLA-PNEUMONIAE, SALMONELLA, SPECTRUM, ENVIRONMENT, REGULATOR, EVOLUTION, PROTEIN, SLYA
  • Hacettepe University Affiliated: Yes

Abstract

Antibiotic resistance is a major problem for public health worldwide. Since bacteria may rapidly respond to antibiotics and acquire resistance, it is important to understand how the bacterial genome changes under antibiotic treatments. With the advent of high-throughput approaches, experimental limitations in characterizing the roles of new mutations and the selection related to the evolution of antibiotic resistance have been eliminated. Here, to explore the mutation profiles of E. coli populations exposed to sub-inhibitory and then increasing concentrations of the antibiotics norfloxacin and colistin, an evolution experiment was combined with whole-population genomic sequencing. The results showed that, while the occurrence of genome-wide mutations is dramatically higher in the populations that were only treated with norfloxacin, there is a remarkable decrease in the colistin-treated populations compared to norfloxacin. It suggests that antibiotics not only elevate the genome-wide mutation rate but also magnify the rate of occurrence of advantageous mutations that increase the rate of adaptation. This work provides further evidence to support the idea that antibiotics can act indirectly as bacterial mutagens, and also that sequential antibiotic treatments may contribute to acquiring antibiotic resistance by improving the adaptation rate in bacteria in a relatively short time.