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      Antiviral Interferon-Beta Signaling Induced by Designed Transcription Activator-Like Effectors (TALE)

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          Abstract

          Here we show that designed transcription activator-like effectors (TALEs) that bind to defined areas of the interferon beta promoter are capable to induce IFN-beta expression and signaling in human cells. Importantly, TALE-mediated IFN-beta signaling occurs independently of pathogen pattern recognition but effectively prohibits viral RNA replication as demonstrated with a hepatitis C virus replicon. TALEs were thus indicated to be valuable tools in various applications addressing, for example, virus-host interactions.

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          Most cited references15

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          Xanthomonas AvrBs3 family-type III effectors: discovery and function.

          Jens Boch, Ulla Bonas (2010)
          Xanthomonads are bacterial plant pathogens that cause diseases on many plant species, including important crops. Key to pathogenicity of most Xanthomonas pathovars is a Hrp-type III secretion (T3S) system that translocates effector proteins into plant cells. Within the eukaryotic cell, the effectors are thought to perform a variety of tasks to support bacterial virulence, proliferation, and dissemination. We are only beginning to understand the host targets of different effectors. The largest effector family found in Xanthomonas spp. is the AvrBs3/PthA or TAL (transcription activator-like) family. TAL effectors act as transcriptional activators in the plant cell nucleus. Specificity of TAL effectors is determined by a novel modular DNA-binding domain. Here, we describe the discovery of TAL effectors and their structure, activity, and host targets.
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            Programmable Sequence-Specific Transcriptional Regulation of Mammalian Genome Using Designer TAL Effectors

            Feng Zhang, Le Cong, Simona Lodato … (2011)
            The ability to direct functional domains to specific DNA sequences is a long sought-after goal for studying and engineering biological processes. Transcription activator like effectors (TALEs) from Xanthomonas sp. present a promising platform for designing sequence-specific DNA binding proteins. Here we describe a robust and rapid method for overcoming the difficulty of constructing TALE repeat domains. We synthesized 17 designer TALEs (dTALEs) that are customized to recognize specific DNA binding sites, and demonstrate that dTALEs can specifically modulate transcription of endogenous genes (Sox2 and Klf4) from the native genome in human cells. dTALEs provide a designable DNA targeting platform for the interrogation and engineering of biological systems.
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              Regulating intracellular antiviral defense and permissiveness to hepatitis C virus RNA replication through a cellular RNA helicase, RIG-I.

              Rhea Sumpter, Yueh-Ming Loo, Eileen Foy … (2005)
              Virus-responsive signaling pathways that induce alpha/beta interferon production and engage intracellular immune defenses influence the outcome of many viral infections. The processes that trigger these defenses and their effect upon host permissiveness for specific viral pathogens are not well understood. We show that structured hepatitis C virus (HCV) genomic RNA activates interferon regulatory factor 3 (IRF3), thereby inducing interferon in cultured cells. This response is absent in cells selected for permissiveness for HCV RNA replication. Studies including genetic complementation revealed that permissiveness is due to mutational inactivation of RIG-I, an interferon-inducible cellular DExD/H box RNA helicase. Its helicase domain binds HCV RNA and transduces the activation signal for IRF3 by its caspase recruiting domain homolog. RIG-I is thus a pathogen receptor that regulates cellular permissiveness to HCV replication and, as an interferon-responsive gene, may play a key role in interferon-based therapies for the treatment of HCV infection.
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                Author and article information

                Contributors
                Matthias J. Schnell: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, USA )
                ISSN (Electronic): 1932-6203
                Publication date Collection: 2014
                Publication date (Electronic): 3 December 2014
                Volume: 9
                Issue: 12
                Electronic Location Identifier: e114288
                Affiliations
                [1]Institute of Biochemistry and Biotechnology, Section Microbial Biotechnology, Martin Luther University Halle-Wittenberg, Faculty of Life Sciences (NFI), Kurt-Mothes-Str. 3, D-06120, Halle/Saale, Germany
                Thomas Jefferson University, United States of America
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Conceived and designed the experiments: IR RG SF SEB. Performed the experiments: IR NF RG SF AP. Analyzed the data: IR NF RG SF SEB. Contributed to the writing of the manuscript: SEB.

                Article
                Publisher ID: PONE-D-14-26487
                DOI: 10.1371/journal.pone.0114288
                PMC ID: 4255017
                PubMed ID: 25470486
                SO-VID: ac0be71a-e478-4473-83ad-8e7d00637f24
                Copyright statement: Copyright @ 2014
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 19 June 2014
                Date accepted : 7 November 2014
                Page count
                Pages: 8
                Funding
                This study was supported by the Deutsche Forschungsgemeinschaft (BE 1885/9-1). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Research Article
                Subject: Biology and life sciences
                Subject: Biochemistry
                Subject: Proteins
                Subject: Interferons
                Subject: Immunology
                Subject: Vaccination and Immunization
                Subject: Antiviral Therapy
                Subject: Microbiology
                Subject: Medical microbiology
                Subject: Microbial pathogens
                Subject: Viral pathogens
                Subject: Flaviviruses
                Subject: Hepatitis C virus
                Subject: Hepatitis Viruses
                Subject: Virology
                Subject: Viral Immune Evasion
                Custom metadata
                Data Availability The authors confirm that all data underlying the findings are fully available without restriction. All relevant data are within the paper and its Supporting Information files.

                ScienceOpen disciplines: Uncategorized
                Data availability:
                ScienceOpen disciplines: Uncategorized

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