| Project/Area Number |
10680694
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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 |
Developmental biology
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| Research Institution | The Institute of Physical and Chemical Research, RIKEN |
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Principal Investigator |
AKIMARU Hiroshi Laboratory of Moleular and Genetics, Senior Research Schientist, 分子遺伝学研究室, 先任研究員 (70241247)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 1999: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1998: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | Drosophila / transcription factor / eye imaginal disc / cell cycle / dmyb / dmi-2 / mosaic analysis / Myb / Mi-2 / 複眼 / 分子遺伝学 |
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| Research Abstract |
To elucidate the function of the D-myb gene encoding a transcription factor in Drosophia, we isolated the D-myb mutant and used it to induce the mutant cells homozygous for the D-myb gene by the mosaic analysis into the eye imaginal disc in which the patterns of cell cycle are definitely controlled. We examined the incorporation of BrdU as a marker for S phase and the expression of the cycline B gene as a marker for G2-M transition within the D-myb mutant clones. The incorporation of BrdU and the expression of the cycline B gene could not be seen within the D-myb mutant clones, suggesting that the D-myb is involved in both the progression of S phase and the transition of G2-M phase. Furthermore, for the isolation of factors in the D-myb signal pathway by the genetic approach, we constructed the transgenic fly specifically expressing the constitutive active form of D-myb, dmyb-TA, deleted the negative regulatory domain at the C-terminal region in the eye imaginal disc. This fly shows the rough eye phenotype due to the ectopic G2-M transition. We have genetically screened the modifier mutants of the rough eye phenotype in the dmyb-TA transgenic fly, resulted in the isolation of three mutants suppressed the rough eye phenotype. One of them was the dmi-2 mutant which has been known to function as a transcriptional repressor. Like the D-myb mutant clones, the expression of the cycline B gene was not induced within the dmi-2 mutant clones. We demonstrated the direct interaction between the dMyb and dMi-2 proteins by GST pull-down binding assay. These findings suggest that the dMi-2 does not function as the repressor for the transcriptional activity of the D-Myb but as the activator.
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