Abstract
Networks of interacting transcription factors are central to the regulation of cellular responses to abiotic stress. Although the architecture of many such networks has been mapped, their dynamic function remains unclear. Here we address this challenge in archaea, microorganisms possessing transcription factors that resemble those of both eukaryotes and bacteria. Using genome-wide DNA binding location analysis integrated with gene expression and cell physiological data, we demonstrate that a bacterial-type transcription factor (TF), called RosR, and five TFIIB proteins, homologs of eukaryotic TFs, combinatorially regulate over 100 target genes important for the response to extremely high levels of peroxide. These genes include 20 other transcription factors and oxidative damage repair genes. RosR promoter occupancy is surprisingly dynamic, with the pattern of target gene expression during the transition from rapid growth to stress correlating strongly with the pattern of dynamic binding. We conclude that a hierarchical regulatory network orchestrated by TFs of hybrid lineage enables dynamic response and survival under extreme stress in archaea. This raises questions regarding the evolutionary trajectory of gene networks in response to stress.
Highlights
All organisms encounter reactive oxygen species (ROS) originating from biotic and abiotic sources
The wiring of many of these circuits has been mapped, how circuits operate in real time to carry out their functions is poorly understood. We address these questions by investigating the function of a gene circuit that responds to reactive oxygen species damage in archaea, microorganisms that represent the third domain of life
Components of archaeal regulatory machinery driving gene circuits resemble those of both bacteria and eukaryotes
Summary
All organisms encounter reactive oxygen species (ROS) originating from biotic and abiotic sources. Oxidants must be neutralized and macromolecular damage repaired at the cellular level to enable survival Enzymes such as superoxide dismutase and thioredoxin reductase are induced to neutralize oxidants and restore redox balance in the cell [4]. The production of these oxidant response proteins is typically transient and precisely controlled to enable rapid restoration of homeostasis following oxidant clearance and damage repair [5]. Such regulation is accomplished by a diversity of strategies throughout the microbial world. TFs [7,8] or their bound cofactors [9,10] are directly and reversibly oxidized in the presence of ROS, altering DNA binding specificity to induce repair enzyme-coding genes [5,11]
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