The Redox System in C. elegans, a Phylogenetic Approach

Oxidative stress is a toxic state caused by an imbalance between the production and elimination of reactive oxygen species (ROS). ROS cause oxidative damage to cellular components such as proteins, lipids, and nucleic acids. While the role of ROS in cellular damage is frequently all that is noted, R...

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Main Authors: Andrew D. Johnston, Paul R. Ebert
Format: Article
Language:English
Published: Wiley 2012-01-01
Series:Journal of Toxicology
Online Access:http://dx.doi.org/10.1155/2012/546915
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author Andrew D. Johnston
Paul R. Ebert
author_facet Andrew D. Johnston
Paul R. Ebert
author_sort Andrew D. Johnston
collection DOAJ
description Oxidative stress is a toxic state caused by an imbalance between the production and elimination of reactive oxygen species (ROS). ROS cause oxidative damage to cellular components such as proteins, lipids, and nucleic acids. While the role of ROS in cellular damage is frequently all that is noted, ROS are also important in redox signalling. The “Redox Hypothesis" has been proposed to emphasize a dual role of ROS. This hypothesis suggests that the primary effect of changes to the redox state is modified cellular signalling rather than simply oxidative damage. In extreme cases, alteration of redox signalling can contribute to the toxicity of ROS, as well as to ageing and age-related diseases. The nematode species Caenorhabditis elegans provides an excellent model for the study of oxidative stress and redox signalling in animals. We use protein sequences from central redox systems in Homo sapiens, Drosophila melanogaster, and Saccharomyces cerevisiae to query Genbank for homologous proteins in C. elegans. We then use maximum likelihood phylogenetic analysis to compare protein families between C. elegans and the other organisms to facilitate future research into the genetics of redox biology.
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spelling doaj-art-a03302687984458490099dff33159edf2025-02-03T05:48:06ZengWileyJournal of Toxicology1687-81911687-82052012-01-01201210.1155/2012/546915546915The Redox System in C. elegans, a Phylogenetic ApproachAndrew D. Johnston0Paul R. Ebert1School of Biological Sciences, The University of Queensland, St Lucia, QLD 4072, AustraliaSchool of Biological Sciences, The University of Queensland, St Lucia, QLD 4072, AustraliaOxidative stress is a toxic state caused by an imbalance between the production and elimination of reactive oxygen species (ROS). ROS cause oxidative damage to cellular components such as proteins, lipids, and nucleic acids. While the role of ROS in cellular damage is frequently all that is noted, ROS are also important in redox signalling. The “Redox Hypothesis" has been proposed to emphasize a dual role of ROS. This hypothesis suggests that the primary effect of changes to the redox state is modified cellular signalling rather than simply oxidative damage. In extreme cases, alteration of redox signalling can contribute to the toxicity of ROS, as well as to ageing and age-related diseases. The nematode species Caenorhabditis elegans provides an excellent model for the study of oxidative stress and redox signalling in animals. We use protein sequences from central redox systems in Homo sapiens, Drosophila melanogaster, and Saccharomyces cerevisiae to query Genbank for homologous proteins in C. elegans. We then use maximum likelihood phylogenetic analysis to compare protein families between C. elegans and the other organisms to facilitate future research into the genetics of redox biology.http://dx.doi.org/10.1155/2012/546915
spellingShingle Andrew D. Johnston
Paul R. Ebert
The Redox System in C. elegans, a Phylogenetic Approach
Journal of Toxicology
title The Redox System in C. elegans, a Phylogenetic Approach
title_full The Redox System in C. elegans, a Phylogenetic Approach
title_fullStr The Redox System in C. elegans, a Phylogenetic Approach
title_full_unstemmed The Redox System in C. elegans, a Phylogenetic Approach
title_short The Redox System in C. elegans, a Phylogenetic Approach
title_sort redox system in c elegans a phylogenetic approach
url http://dx.doi.org/10.1155/2012/546915
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