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      Duox is the primary NADPH oxidase responsible for ROS production during adult caudal fin regeneration in zebrafish

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          Summary

          Sustained elevated levels of reactive oxygen species (ROS) have been shown to be essential for regeneration in many organisms. This has been shown primarily via the use of pharmacological inhibitors targeting the family of NADPH oxidases (NOXes). To identify the specific NOXes involved in ROS production during adult caudal fin regeneration in zebrafish, we generated nox mutants for duox, nox5 and cyba (a key subunit of NOXes 1–4) and crossed these lines with a transgenic line ubiquitously expressing HyPer, which permits the measurement of ROS levels. Homozygous duox mutants had the greatest effect on ROS levels and rate of fin regeneration among the single mutants. However, duox: cyba double mutants showed a greater effect on fin regeneration than the single duox mutants, suggesting that Nox1-4 also play a role during regeneration. This work also serendipitously found that ROS levels in amputated adult zebrafish fins oscillate with a circadian rhythm.

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          Highlights

          • •

            Fin amputation results in elevated ROS that oscillate with the circadian clock

          • •

            duox mutants have diminished ROS levels following caudal fin amputation

          • •

            duox mutants have diminished rate of caudal fin regeneration

          • •

            duox/cyba mutants have a more severe defect in regeneration than duox mutants

          Abstract

          Cell biology; Ichthyology; Molecular genetics

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          The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology.

          Karen Bedard, Karl-Heinz Krause (2007)
          For a long time, superoxide generation by an NADPH oxidase was considered as an oddity only found in professional phagocytes. Over the last years, six homologs of the cytochrome subunit of the phagocyte NADPH oxidase were found: NOX1, NOX3, NOX4, NOX5, DUOX1, and DUOX2. Together with the phagocyte NADPH oxidase itself (NOX2/gp91(phox)), the homologs are now referred to as the NOX family of NADPH oxidases. These enzymes share the capacity to transport electrons across the plasma membrane and to generate superoxide and other downstream reactive oxygen species (ROS). Activation mechanisms and tissue distribution of the different members of the family are markedly different. The physiological functions of NOX family enzymes include host defense, posttranlational processing of proteins, cellular signaling, regulation of gene expression, and cell differentiation. NOX enzymes also contribute to a wide range of pathological processes. NOX deficiency may lead to immunosuppresion, lack of otoconogenesis, or hypothyroidism. Increased NOX activity also contributes to a large number or pathologies, in particular cardiovascular diseases and neurodegeneration. This review summarizes the current state of knowledge of the functions of NOX enzymes in physiology and pathology.
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            A tissue-scale gradient of hydrogen peroxide mediates rapid wound detection in zebrafish

            Philipp Niethammer, Clemens Grabher, A. Thomas Look … (2009)
            Barrier structures (e.g. epithelia around tissues, plasma membranes around cells) are required for internal homeostasis and protection from pathogens. Wound detection and healing represent a dormant morphogenetic program that can be rapidly executed to restore barrier integrity and tissue homeostasis. In animals, initial steps include recruitment of leukocytes to the site of injury across distances of hundreds of micrometers within minutes of wounding. The spatial signals that direct this immediate tissue response are unknown. Due to their fast diffusion and versatile biological activities, reactive oxygen species (ROS), including hydrogen peroxide (H2O2), are interesting candidates for wound-to-leukocyte signalling. We probed the role of H2O2 during the early events of wound responses in zebrafish larvae expressing a genetically encoded H2O2 sensor1. This reporter revealed a sustained rise in H2O2 concentration at the wound margin, starting ∼3 min after wounding and peaking at ∼20 min, which extended ∼100−200 μm into the tail fin epithelium as a decreasing concentration gradient. Using pharmacological and genetic inhibition, we show that this gradient is created by Dual oxidase (Duox), and that it is required for rapid recruitment of leukocytes to the wound. This is the first observation of a tissue-scale H2O2 pattern, and the first evidence that H2O2 signals to leukocytes in tissues, in addition to its known antiseptic role.
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              Genetic compensation triggered by mutant mRNA degradation

              Mohamed El-Brolosy, Zacharias Kontarakis, Andrea Rossi … (2019)
              Genetic robustness, or the ability of an organism to maintain fitness in the presence of mutations, can be achieved via protein feedback loops. Recent evidence suggests that organisms may also respond to mutations by upregulating related gene(s) independently of protein feedback loops, a phenomenon called transcriptional adaptation. However, the prevalence of transcriptional adaptation and its underlying molecular mechanisms are unknown. Here, by analyzing several models of transcriptional adaptation in zebrafish and mouse, we show a requirement for mRNA degradation. Alleles that fail to transcribe the mutated gene do not display transcriptional adaptation and exhibit more severe phenotypes than alleles displaying mutant mRNA decay. Transcriptome analysis reveals the upregulation of a substantial proportion of the genes that exhibit sequence similarity with the mutated gene’s mRNA, suggesting a sequence dependent mechanism. Besides implications for our understanding of disease-causing mutations, these findings will help design mutant alleles with minimal transcriptional adaptation-derived compensation.
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                Author and article information

                Contributors
                Enrique Amaya
                Journal
                Journal ID (nlm-ta): iScience
                Journal ID (iso-abbrev): iScience
                Title: iScience
                Publisher: Elsevier
                ISSN (Electronic): 2589-0042
                Publication date PMC-release: 04 February 2023
                Publication date Collection: 17 March 2023
                Publication date (Electronic): 04 February 2023
                Volume: 26
                Issue: 3
                Electronic Location Identifier: 106147
                Affiliations
                [1 ]Division of Cell Matrix Biology & Regenerative Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, UK
                [2 ]Manchester Fungal Infection Group (MFIG), Division of Evolution, Infection, and Genomics, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, UK
                [3 ]Mycology Reference Laboratory, National Centre for Microbiology, Instituto de Salud Carlos III (ISCIII), Majadahonda 28220 Madrid, Spain
                Author notes
                [∗ ]Corresponding author enrique.amaya@ 123456manchester.ac.uk
                [4]

                Present address: Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, UK

                [5]

                Lead contact

                Article
                Publisher Item ID: S2589-0042(23)00224-9 Publisher ID: 106147
                DOI: 10.1016/j.isci.2023.106147
                PMC ID: 9950526
                PubMed ID: 36843843
                SO-VID: 0c88fc1b-88d5-434b-979d-64da0f75e1fd
                Copyright © © 2023 The Authors.
                License:

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 26 April 2022
                Date revision received : 28 November 2022
                Date accepted : 1 February 2023
                Categories
                Subject: Article

                Keywords: cell biology,ichthyology,molecular genetics
                Data availability:
                Keywords: cell biology, ichthyology, molecular genetics

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