Abstract
90% of the world population is exposed to heavy atmospheric pollution. This is a major public health issue causing 7 million death each year. Air pollution comprises an array of pollutants such as particulate matters, ozone and carbon monoxide imposing a multifactorial stress on living cells. Here, Escherichia coli was used as model cell and adapted for 390 generations to atmospheric pollution to assess its long-term effects at the genetic, transcriptomic and physiological levels. Over this period, E. coli evolved to grow faster and acquired an adaptive mutation in rpoB, which encodes the RNA polymerase β subunit. Transcriptomic and biochemical characterization showed alteration of the cell membrane composition resulting in lesser permeability after the adaptation process. A second significant change in the cell wall structure of the adapted strain was the greater accumulation of the exopolysaccharides colanic acid and cellulose in the extracellular fraction. Results also indicated that amino acids homeostasis was involved in E. coli response to atmospheric pollutants. This study demonstrates that adaptive mutation with transformative physiological impact can be fixed in genome after exposure to atmospheric pollution and also provides a comprehensive portrait of the cellular response mechanisms involved.
Highlights
9 out of 10 persons are breathing heavily polluted air worldwide[1]
Bacterial cultures were grown under standard laboratory atmosphere (SLA), urban polluted atmosphere with a PM2.5 concentration of 230 μg m−3 (UPA230) considered as very unhealthy or under diesel exhaust atmosphere with a PM2.5 concentration of 613 μg m−3 (DEA613), which is outside the air quality index range (AQI) (Table 1)
When the same strain was grown under DEA613, doubling time was 1.6 time slower compared to Standard laboratory air (SLA)-grown wt cultures
Summary
9 out of 10 persons are breathing heavily polluted air worldwide[1]. Morbidity and mortality have been shown to be increased after exposure to fine particulate matter (PM) found in air pollution[2,3]. Fine PM, which is considered to be the principal factor responsible for the relation between atmospheric pollution and morbidity, affects health negatively via multiple mechanisms such as genotoxicity, inflammation, cell death, procoagulant effects and reactive oxygen species (ROS)[6,7]. Air pollution composition varies significantly depending on the geographical area, the season and the source of pollutants[8] It contains PM with a diameter between 2.5 to 10 μM (PM10), PM below 2.5 μM (PM2.5), ultrafine PM (PM0.1), ozone, carbon monoxide, nitrogen oxides, sulfur oxides, metals, organic compounds and biological matter[9]. ALE mainly consists in cultivating an organism under specific conditions over multiple generations[29] During this process, mutations occur and beneficial ones are fixed in the genome[21]. ALE in combination with genome sequencing and transcriptomic has been used to study the impact of stresses such as alcohol, temperature, UV light, osmotic pressure and antibiotic on prokaryotic as well eukaryotic cells[30,31,32,33,34]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
