Antibiotic tolerance and degradation capacity of the organic pollutant-degrading bacterium Rhodococcus biphenylivorans TG9T

Antibiotics are ubiquitous in soil due to natural ecological competition, as well as emerging contaminants due to anthropogenic inputs. Under environmental factors like antibiotic stress, some bacteria, including those that degrade environmental pollutants, can enter a dormant state as a survival strategy, thereby limiting their metabolic activity and function. Dormancy has a critical influence on the degradative activity of bacteria, dramatically decreasing the rate at which they transform organic pollutants. To better understand this phenomenon in environmental pollutant-degrading bacteria, we investigated dormancy transitions induced with norfloxacin in Rhodococcus biphenylivorans TG9T using next-generation proteomics, proteogenomics, and additional experiments. Our results suggest that exposure to norfloxacin inhibited DNA replication, which led to damage to the cell. Dormant cells then likely triggered DNA repair, particularly homologous recombination, for continued survival. The results also indicated that substrate transport (ATP-binding cassette transporter), ATP production, and the tricarboxylic acid (TCA) cycle were repressed during dormancy, and degradation of organic pollutants was down-regulated. Given the widespread phenomenon of dormancy among bacteria involved in pollutant removal systems, this study improves our understanding of possible implications of antibiotic survival strategies on biotransformation of mixtures containing antibiotics as well as other organics.

Automated summary

Antibiotics are widespread in soil, influencing bacteria involved in pollutant removal systems. Exposure to antibiotics can lead to dormancy in bacteria, affecting their degradative activity. The study found that antibiotic exposure inhibits DNA replication, triggering DNA repair in dormant cells for survival.