Genetic approaches to elucidate mechanism for action of dioxin receptor using Drosophila
| Project/Area Number |
15510052
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Risk sciences of radiation/Chemicals
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| Research Institution | Kobe University |
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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)
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| Project Period (FY) |
2003 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| 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)
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| Keywords | Drosophila / Dioxin receptor / apoptosis / homeotic transformation / genetics / JNK / LRR protein / cell-cell interaction / アポトーシス / 器官形成 |
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| 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.
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Report
(4 results)
Research Products
(5 results)
