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Genetic approaches to elucidate mechanism for action of dioxin receptor using Drosophila

Research Project

Project/Area Number 15510052
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Risk sciences of radiation/Chemicals
Research InstitutionKobe University

Principal Investigator

ADACHI Takashi  Kobe University, Graduate School of Science and Technology, Associate Professor, 自然科学研究科, 助教授 (20221723)

Project Period (FY) 2003 – 2005
Project Status Completed (Fiscal Year 2005)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2004: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2003: ¥2,100,000 (Direct Cost: ¥2,100,000)
KeywordsDrosophila / Dioxin receptor / apoptosis / homeotic transformation / genetics / JNK / LRR protein / cell-cell interaction / アポトーシス / 器官形成
Research Abstract

Dioxins show a chronic toxicity, teratogenicity and carcinogenicity. Its atmospheric accumulation is therefore one of the current environmental problems to be resolved. Intracellular dioxins bind to its receptor Ahr which is a transcription factor and act together with an allied protein Arnt. However the pathways regulating apoptosis, teratogenicity, and carcinogenicity have not fully been revealed. We have thus used a genetically amenable model organism Drosophila to clarify these mechanisms. We found that ectopic action of Spineless, a Drosophila homolog of dioxin receptor induces a severe apoptosis. Using this phenotype, we tried to study about the following three issues.
1. Analysis of signaling pathways to lead to apoptosis induced by Spineless.
2. Effect of JNK, a environmental stress-activated signal transducer, on action of Spineless.
3. Isolation and analysis of new mutant which suppresses apoptosis induced by Spineless.
Results :
1. Ectopic action of Spineless in the wing leads to ectopic occurrence of the leg/antenna through elevation of Distal-less expression. The apoptosis is dependent on this homeotic transformation. The key to induce apoptosis is reduction of cell-cell interaction mediated by a novel LRR family protein Fish-lips.
2. Apoptosis induced by Spineless strongly depends on JNK activity, whereas both the homeotic transformation and alteration of cell-cell interaction by Spineless were not affected by JNK.
3. A novel mutant "Suppressor of spineless expression (Sussex)" was isolated and mapped to the second chromosome.

Report

(4 results)
  • 2005 Annual Research Report   Final Research Report Summary
  • 2004 Annual Research Report
  • 2003 Annual Research Report
  • Research Products

    (5 results)

All 2005 2004

All Journal Article (5 results)

  • [Journal Article] Wing-to-leg homeosis by Spineless causes apoptosis regulated by Fish-lips, a novel Leucine-Rich Repeat Transmembrane Protein2005

    • Author(s)
      Takashi Adachi-Yamada
    • Journal Title

      Molecular and Cellular Biology 25(8)

      Pages: 3140-3150

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Wing-to-leg homeosis by Spineless causes apoptosis regulated by Fish-lips, a novel Leucine-Rich Repeat Transmembrane Protein2005

    • Author(s)
      Takashi, Adachi-Yamada et al.
    • Journal Title

      Mol.Cell.Biol. 25(8)

      Pages: 3140-3150

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Wing-to-leg homeosis by Spineless causes apoptosis regulated by Fish-lips, a novel Leucine-Rich Repeat Transmembrane Protein2005

    • Author(s)
      Takashi Adachi-Yamada
    • Journal Title

      Molecular and Cellular Biology 25(8)(印刷中)

    • Related Report
      2005 Annual Research Report 2004 Annual Research Report
  • [Journal Article] Mechanisms for removal of developmentally abnormal cells : cell competition and morphogenetic apoptosis2004

    • Author(s)
      Takashi Adachi-Yamada, Michael B. O' Connor
    • Journal Title

      Journal of Biochemistry (Tokyo) 136

      Pages: 13-17

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Mechanisms for removal of developmentally abnormal cells: cell competition and morphogenetic apoptosis2004

    • Author(s)
      Takashi Adachi-Yamada, Michael B.O'Connor
    • Journal Title

      J.Biochem.(Tokyo) 136

      Pages: 13-17

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2005 Final Research Report Summary

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Published: 2003-04-01   Modified: 2016-04-21  

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