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      Generation of medaka gene knockout models by target-selected mutagenesis

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          Abstract

          A reverse genetics approach for the routine generation of medaka ( Oryzias latipes) gene knockouts is described and applied to create a cryopreserved resource containing knockouts for most medaka genes.

          Abstract

          We have established a reverse genetics approach for the routine generation of medaka ( Oryzias latipes) gene knockouts. A cryopreserved library of N-ethyl- N-nitrosourea (ENU) mutagenized fish was screened by high-throughput resequencing for induced point mutations. Nonsense and splice site mutations were retrieved for the Blm, Sirt1, Parkin and p53 genes and functional characterization of p53 mutants indicated a complete knockout of p53 function. The current cryopreserved resource is expected to contain knockouts for most medaka genes.

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          Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours.

          L A Donehower, M. Harvey, B Slagle … (1992)
          Mutations in the p53 tumour-suppressor gene are the most frequently observed genetic lesions in human cancers. To investigate the role of the p53 gene in mammalian development and tumorigenesis, a null mutation was introduced into the gene by homologous recombination in murine embryonic stem cells. Mice homozygous for the null allele appear normal but are prone to the spontaneous development of a variety of neoplasms by 6 months of age. These observations indicate that a normal p53 gene is dispensable for embryonic development, that its absence predisposes the animal to neoplastic disease, and that an oncogenic mutant form of p53 is not obligatory for the genesis of many types of tumours.
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            Nonsense-mediated mRNA decay: splicing, translation and mRNP dynamics.

            Lynne Maquat (2004)
            Studies of nonsense-mediated mRNA decay in mammalian cells have proffered unforeseen insights into changes in mRNA-protein interactions throughout the lifetime of an mRNA. Remarkably, mRNA acquires a complex of proteins at each exon-exon junction during pre-mRNA splicing that influences the subsequent steps of mRNA translation and nonsense-mediated mRNA decay. Complex-loaded mRNA is thought to undergo a pioneer round of translation when still bound by cap-binding proteins CBP80 and CBP20 and poly(A)-binding protein 2. The acquisition and loss of mRNA-associated proteins accompanies the transition from the pioneer round to subsequent rounds of translation, and from translational competence to substrate for nonsense-mediated mRNA decay.
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              The Bloom's syndrome gene product is homologous to RecQ helicases.

              N A Ellis, J Groden, T Ye … (1995)
              The Bloom's syndrome (BS) gene, BLM, plays an important role in the maintenance of genomic stability in somatic cells. A candidate for BLM was identified by direct selection of a cDNA derived from a 250 kb segment of the genome to which BLM had been assigned by somatic crossover point mapping. In this novel mapping method, cells were used from persons with BS that had undergone intragenic recombination within BLM. cDNA analysis of the candidate gene identified a 4437 bp cDNA that encodes a 1417 amino acid peptide with homology to the RecQ helicases, a subfamily of DExH box-containing DNA and RNA helicases. The presence of chain-terminating mutations in the candidate gene in persons with BS proved that it was BLM.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Genome Biol
                Title: Genome Biology
                Publisher: BioMed Central (London )
                ISSN (Print): 1465-6906
                ISSN (Electronic): 1465-6914
                Publication date (Print): 2006
                Publication date (Electronic): 8 December 2006
                Volume: 7
                Issue: 12
                Page: R116
                Affiliations
                [1 ]Department of Radiation Genetics, CREST, Japan Science and Technology Laboratory, Kyoto University, Yoshida Konoe, Sakyo-ku, Kyoto 606-8501, Japan
                [2 ]Kondoh Differentiation Signaling Project, Exploratory Research for Advanced Technology (ERATO), Japan Science and Technology Corporation, Yoshida-kawaramachi, Sakyo-ku, Kyoto, 606-8305, Japan
                [3 ]Department of Mutagenesis, Radiation Biology Center, Kyoto University, Yoshida Konoe, Sakyoku, Kyoto 606-8501, Japan
                [4 ]Hubrecht Laboratory, Uppsalalaan, Utrecht, The Netherlands
                [5 ]Department of Integrated Biosciences, The University of Tokyo, 5-1-5 Kashiwa-no-ha, Kashiwa, Chiba 277-8562, Japan
                [6 ]The Institute of Physical and Chemical Research Genomic Sciences Center, RIKEN Yokohama Institute, 1-7-22 Suehiro, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan
                Article
                Publisher ID: gb-2006-7-12-r116
                DOI: 10.1186/gb-2006-7-12-r116
                PMC ID: 1794429
                PubMed ID: 17156454
                SO-VID: 86d2266c-7e8d-4f9f-91b9-696b4813123a
                Copyright © Copyright © 2006 Taniguchi et al.; licensee BioMed Central Ltd.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 15 August 2006
                Date revision received : 1 November 2006
                Date accepted : 8 December 2006
                Categories
                Subject: Method

                ScienceOpen disciplines: Genetics
                Data availability:
                ScienceOpen disciplines: Genetics

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