| Project/Area Number |
14GS0321
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| Research Category |
Grant-in-Aid for Creative Scientific Research
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| Allocation Type | Single-year Grants |
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| Research Institution | National Institute of Genetics |
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Principal Investigator |
KAKUTANI Tetsuji National Institute of Genetics, Department of Integrated Genetics, Professor (20332174)
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| Co-Investigator(Kenkyū-buntansha) |
KINOSHITA Tetsu National Institute of Genetics, Assistant Professor (60342630)
SHIBAHARA Keiichi National Institute of Genetics, Assistant Professor (20263098)
ARAKI Takashi Kyoto University, Graduate School of Biostudies, Professor (00273433)
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| Project Period (FY) |
2002 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥337,350,000 (Direct Cost: ¥278,130,000、Indirect Cost: ¥59,220,000)
Fiscal Year 2006: ¥63,180,000 (Direct Cost: ¥48,600,000、Indirect Cost: ¥14,580,000)
Fiscal Year 2005: ¥63,050,000 (Direct Cost: ¥48,500,000、Indirect Cost: ¥14,550,000)
Fiscal Year 2004: ¥66,690,000 (Direct Cost: ¥51,300,000、Indirect Cost: ¥15,390,000)
Fiscal Year 2003: ¥63,700,000 (Direct Cost: ¥49,000,000、Indirect Cost: ¥14,700,000)
Fiscal Year 2002: ¥80,730,000 (Direct Cost: ¥80,730,000)
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| Keywords | epigenetic / transposon / DNA methylation / Arabidopsis / chromatin / imprinting / genome / flowering / エピジェネティック / 染色体 / ヘテロクロマチン / ピストン / 胚乳 / ヒストン |
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| Research Abstract |
FWA has been identified as the gene responsible for a late-flowering epigenetic trait (Mol Cell 6, 791-). In this project, we examined expression of the FWA gene during normal development. The FWA gene was expressed specifically in endosperm in an imprinted manner. The tissue-specific and imprinted FWA expression depends on DNA methyltransferase MET1 and DNA demethylase DEMETER (Science 303, 521-). It was also shown that FT is the inducer of flowering (Science 309, 1052-), and the FWA affects flowering by inhibiting the FT function at the protein level (Plant Cell Physiol 48, 205-).
We have previously shown that Arabidopsis CACTA transposons are silent in wild type, but they are mobilized in mutant of a chromatin remodeling gene DDM1 (decrease in DNA methylation) (Nature 411, 212-). In this project, we showed that the CACTA transposons transposed in the double mutants of CG methylase MET1 and non-CG methylase CMT3. The results suggest that DNA methylation is necessary for immobilization of this class of transposons (Curr Biol 13, 421-).
Transcription of CACTA was de-repressed by mutations in the MET1 or a chromatin assembly factor FAS (Curr Biol 13, 421-, Genes to Cells 18, 153-). Heterochromatin in CACTA locus or other peri-centromeric sequences was disrupted by the ddml mutation, and this effect was heritable even in the wild type background (EMBO J 21, 6549-). Using this system, we also showed that each of CACTA transposition was not targeted to heterochromatin (Genetics 168, 961-). It is interesting how the transposons accumulate to form the heterochromatin.
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