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Adult kidney functions in mice lacking genes that are essential for kidney development

Research Project

Project/Area Number 17390248
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Kidney internal medicine
Research InstitutionKumamoto University

Principal Investigator

KOBAYASHI Chiyoko  Kumamoto University, Institute of Molecular Embryology and Genetics, Assistant Professor, 発生医学研究センター, 助手 (20342785)

Co-Investigator(Kenkyū-buntansha) NISHINAKAMURA Ryuichi  Kumamoto University, Institute of Molecular Embryology and Genetics, Professor, 発生医学研究センター, 教授 (70291309)
Project Period (FY) 2005 – 2006
Project Status Completed (Fiscal Year 2006)
Budget Amount *help
¥13,800,000 (Direct Cost: ¥13,800,000)
Fiscal Year 2006: ¥6,300,000 (Direct Cost: ¥6,300,000)
Fiscal Year 2005: ¥7,500,000 (Direct Cost: ¥7,500,000)
KeywordsDevelopment / Kidney Development / Knockout mouse
Research Abstract

Our purpose was to generate conditional mutant mice lacking genes that are essential for kidney development, and to analyze renal functions of these mice at an adult stage. As Sall1 is expressed in the metanephric mesenchyme (renal progenitors) and in the adult kidney, we planned to generate mice harboring CreER, which is a fusion protein of Cre recombinase and a mutated estrogen receptor, in the Sall1 locus. When this mouse is crossed with floxed mice of a variety of developmental genes and is stimulated with tamoxifen, a ligand for ER, we could theoretically delete the genes at desired temporal stages. We succeeded in inserting CreER in the Sall1 locus by homologous recombination in embryonic stem cells, generated chimeric mice, and subsequently obtained Sall1 CreER mouse. To test the efficiency of gene excision using this mouse strain, it was crossed with lacZ indicator mouse and was stimulated with tamoxifen. The lacZ staining, however, was faint, indicating the low rate of excision. We then obtained ROSA26CreER mouse which expresses CreER ubiquitously, and crossed with the indicator mouse, but the lacZ staining was still weak. Though it is possible that our protocol of tamoxifen treatment was not optimal, it is likely that the CreER activity was not high enough to efficiently delete genes, because mice expressing unmodified Cre in the Sall1 locus or ubiquitously showed potent gene excision activity as assessed by the lacZ staining. Thus CreER may not be suitable to generate conditional knockout mice. To achieve the initial purpose that is the analysis of renal functions at the adult stage, we are now generating mice in which Sall1 activity is partially restored.

Report

(3 results)
  • 2006 Annual Research Report   Final Research Report Summary
  • 2005 Annual Research Report
  • Research Products

    (6 results)

All 2006 2005

All Journal Article (5 results) Book (1 results)

  • [Journal Article] Identification of multipotent progenitors in the embryonic mouse kidney by a novel colony-forming assay.2006

    • Author(s)
      Kenji Osafune
    • Journal Title

      Development 133

      Pages: 151-161

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Final Research Report Summary 2005 Annual Research Report
  • [Journal Article] The murine homolog of SALL4. a causative gene in Okihiro syndrome, is essential for embryonic stemcell proliferation, and cooperates with Sall1 in anorectal, heart, brain and kidney development2006

    • Author(s)
      Masayo Sakaki-Yumoto
    • Journal Title

      Development 133

      Pages: 3005-3013

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Annual Research Report 2006 Final Research Report Summary
  • [Journal Article] Essential roles of Sall family genes in kidney development.2006

    • Author(s)
      Ryuichi Nishinakamura
    • Journal Title

      J. Physiol Sci. 56

      Pages: 131-136

    • NAID

      10019283262

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] The murine homolog of SALL4. a causative gene in Okihiro syndrome, is essential for embryonic stem cell proliferation, and cooperates with Sall1 in anorectal, heart, brain and kidney development.2006

    • Author(s)
      Masayo Sakaki-Yumoto
    • Journal Title

      Development 3005-3013

      Pages: 3005-3013

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Essential roles of Sall1 in kidney development.2005

    • Author(s)
      Ryuichi Nishinakamura
    • Journal Title

      Kidney International 68

      Pages: 1948-1950

    • Related Report
      2005 Annual Research Report
  • [Book] 再生医療のための発生生物学2006

    • Author(s)
      西中村 隆一
    • Total Pages
      259
    • Publisher
      コロナ社
    • Related Report
      2006 Annual Research Report

URL: 

Published: 2005-04-01   Modified: 2016-04-21  

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