Abstract

Ever since the “great oxidation event,” Earth’s cellular life forms had to cope with the danger of reactive oxygen species (ROS) affecting the integrity of biomolecules and hampering cellular metabolism circuits. Consequently, increasing ROS levels in the biosphere represented growing stress levels and thus shaped the evolution of species. Whether the ROS were produced endogenously or exogenously, different systems evolved to remove the ROS and repair the damage they inflicted. If ROS outweigh the cell’s capacity to remove the threat, we speak of oxidative stress. The injuries through oxidative stress in cells are diverse. This article reviews the damage oxidative stress imposes on the different steps of the central dogma of molecular biology in bacteria, focusing in particular on the RNA machines involved in transcription and translation.

Highlights

  • Sources of Oxidative Stress and the Bacterial Defense Mechanisms Against ThemThe earliest single-celled life forms evolved on Earth in an anoxic environment around 4 billion years ago (Orgel, 1998)

  • While it has been shown before that exchange of Mg2+ ions in the ribosome can have a detrimental effect on rRNA stability (Winter et al, 1997; Polacek and Barta, 1998), research on the specific role of ribosome bound Fe2+ for oxidative lesions generated through localized Fenton reactions is scarce in bacteria

  • Once oxygen levels rose on Earth, bacterial cells had to develop systems to continuously remove endogenously generated reactive oxygen species (ROS) to keep oxidative damage to a minimum

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Summary

Introduction

Sources of Oxidative Stress and the Bacterial Defense Mechanisms Against ThemThe earliest single-celled life forms evolved on Earth in an anoxic environment around 4 billion years ago (Orgel, 1998). Oxidative stress can result in damage of both the backbone and bases of nucleic acids, both free and incorporated oxidized amino acids, as well as cofactors of proteins. To mitigate the damage of oxidative stress on cell biology, different stress response regulons are activated in bacteria, depending on the type of stressor (reviewed in (Imlay, 2015)).

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