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      PRDX1 is essential for the viability and maintenance of reactive oxygen species in chicken DT40

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          Abstract

          Background

          Peroxiredoxin 1 (PRDX1) is a member of a ubiquitous family of thiol peroxidases that catalyze the reduction of peroxides, including hydrogen peroxide. It functions as an antioxidant enzyme, similar to catalase and glutathione peroxidase. PRDX1 was recently shown act as a sensor of reactive oxygen species (ROS) and play a role in ROS-dependent intracellular signaling pathways. To investigate its physiological functions, PRDX1 was conditionally disrupted in chicken DT40 cells in the present study.

          Results

          The depletion of PRDX1 resulted in cell death with increased levels of intracellular ROS. PRDX1-depleted cells did not show the accumulation of chromosomal breaks or sister chromatid exchange (SCE). These results suggest that cell death in PRDX1-depleted cells was not due to DNA damage. 2-Mercaptoethanol protected against cell death in PRDX1-depleted cells and also suppressed elevations in ROS.

          Conclusions

          PRDX1 is essential in chicken DT40 cells and plays an important role in maintaining intracellular ROS homeostasis (or in the fine-tuning of cellular ROS levels). Cells deficient in PRDX1 may be used as an endogenously deregulated ROS model to elucidate the physiological roles of ROS in maintaining proper cell growth.

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          Most cited references32

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          ROS as signalling molecules: mechanisms that generate specificity in ROS homeostasis.

          Benoit D'Autréaux, Michel B. Toledano (2007)
          Reactive oxygen species (ROS) have been shown to be toxic but also function as signalling molecules. This biological paradox underlies mechanisms that are important for the integrity and fitness of living organisms and their ageing. The pathways that regulate ROS homeostasis are crucial for mitigating the toxicity of ROS and provide strong evidence about specificity in ROS signalling. By taking advantage of the chemistry of ROS, highly specific mechanisms have evolved that form the basis of oxidant scavenging and ROS signalling systems.
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            ATM activation by oxidative stress.

            Zhi Guo Guo, Sergei Kozlov, Martin F. Lavin … (2010)
            The ataxia-telangiectasia mutated (ATM) protein kinase is activated by DNA double-strand breaks (DSBs) through the Mre11-Rad50-Nbs1 (MRN) DNA repair complex and orchestrates signaling cascades that initiate the DNA damage response. Cells lacking ATM are also hypersensitive to insults other than DSBs, particularly oxidative stress. We show that oxidation of ATM directly induces ATM activation in the absence of DNA DSBs and the MRN complex. The oxidized form of ATM is a disulfide-cross-linked dimer, and mutation of a critical cysteine residue involved in disulfide bond formation specifically blocked activation through the oxidation pathway. Identification of this pathway explains observations of ATM activation under conditions of oxidative stress and shows that ATM is an important sensor of reactive oxygen species in human cells.
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              Structure, mechanism and regulation of peroxiredoxins

              J Robin Harris, Leslie Poole, Zachary A Wood … (2003)
              Article 0 comments Cited 227 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Takahito Moriwaki: moriwaki@med.kawasaki-m.ac.jp
                Akari Yoshimura: akari-yo@tohoku-mpu.ac.jp
                Yuki Tamari: tamari@koto.kpu-m.ac.jp
                Hiroyuki Sasanuma: hiroysasa@rg.med.kyoto-u.ac.jp
                Shunichi Takeda: takeda.shunichi.5c@kyoto-u.jp
                Masayuki Seki: seki@tohoku-mpu.ac.jp
                Keizo Tano:
                ORCID: http://orcid.org/0000-0003-3900-0035
                tano.keizo.y90@kyoto-u.jp
                Journal
                Journal ID (nlm-ta): Genes Environ
                Journal ID (iso-abbrev): Genes Environ
                Title: Genes and Environment
                Publisher: BioMed Central (London )
                ISSN (Print): 1880-7046
                ISSN (Electronic): 1880-7062
                Publication date (Electronic): 5 August 2021
                Publication date PMC-release: 5 August 2021
                Publication date Collection: 2021
                Volume: 43
                Electronic Location Identifier: 35
                Affiliations
                [1 ]Department of Molecular and Genetic Medicine, Kawasaki Medical School, 577, Matsushima, Kurashiki-city, Okayama 701-0192 Japan
                [2 ]GRID grid.412755.0, ISNI 0000 0001 2166 7427, Division of Biochemistry, Faculty of Pharmaceutical Sciences, , Tohoku Medical and Pharmaceutical University, ; 4-4-1 Komatsushima, Aoba-ku, Sendai, Miyagi 981-8558 Japan
                [3 ]GRID grid.272458.e, ISNI 0000 0001 0667 4960, Department of Radiology, , Kyoto Prefectural University of Medicine, ; Kajii-cho, Kawaramachi-Hirokoji,Kamigyo-ku, Kyoto, 602-8566 Japan
                [4 ]GRID grid.258799.8, ISNI 0000 0004 0372 2033, Department of Radiation Genetics, Graduate School of Medicine, Faculty of Medicine, , Kyoto University, ; Yoshida-Konoe-cho, Sakyo-ku, Kyoto, 606-8501 Japan
                [5 ]GRID grid.261455.1, ISNI 0000 0001 0676 0594, Department of Biological Sciences, Graduate School of Science, , Osaka Prefecture University, ; 1-1 Gakuen-cho, Naka-ku, Sakai, Osaka, 599-8531 Japan
                Author information
                http://orcid.org/0000-0003-3900-0035
                Article
                Publisher ID: 211
                DOI: 10.1186/s41021-021-00211-4
                PMC ID: 8340460
                PubMed ID: 34353368
                SO-VID: e1cffb40-f3da-4fad-b469-7c7c87c194e4
                Copyright © © The Author(s) 2021
                License:

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                Date received : 5 May 2021
                Date accepted : 26 July 2021
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001691, Japan Society for the Promotion of Science;
                Award ID: 18K11640
                Award Recipient :
                Categories
                Subject: Research
                Custom metadata
                issue-copyright-statement © The Author(s) 2021

                Data availability:

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