| Project/Area Number |
15207005
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
植物生理・分子
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| Research Institution | National Institute for Basic Biology (2004-2005)
Okazaki National Research Institutes (2003) |
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Principal Investigator |
NISHIMURA Mikio National Institute for Basic Biology, Department of Cell Biology, Professor, 高次細胞機構研究部門, 教授 (80093061)
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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 |
¥49,530,000 (Direct Cost: ¥38,100,000、Indirect Cost: ¥11,430,000)
Fiscal Year 2005: ¥13,520,000 (Direct Cost: ¥10,400,000、Indirect Cost: ¥3,120,000)
Fiscal Year 2004: ¥12,740,000 (Direct Cost: ¥9,800,000、Indirect Cost: ¥2,940,000)
Fiscal Year 2003: ¥23,270,000 (Direct Cost: ¥17,900,000、Indirect Cost: ¥5,370,000)
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| Keywords | peroxisome / glyoxysome / Arabidopsis thaliana / mitochondria / organelle differentiation / apm mutants / peroxin / protein traffic / ペルオキシソーム形成 / ペルオキシソーム形成因子 / PTS1タンパク質輸送 / PTS2タンパク質輸送 / ペルオキシソームの分裂 / ミトコンドリアの分裂 / DRP3A / プロテオーム / トランスクリプトーム / 緑葉ペルオキシソーム |
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| Research Abstract |
Peroxisomes in higher plantcells are known to differentiate in function depending on the cell type. By a comprehensive survey of peroxisomal genes in the entire Arabidopsis genome, we found 286 candidates of peroxisomal genes. They included all genes for peroxisomal enzymes reported up to date, and most of them encoded functionally unknown proteins in peroxisomes. Analyses of gene expression profiles revealed that peroxisomal differentiation is caused by the expression of specific genes that are induced in specific organs in addition to constitutively expressed genes. The clustering analyses suggested that basic functions of peroxisomewereβ-oxidation, H_2O_2 degradation, branched chain amino acid catabolism and some unknown functions, and that peroxisomesinseedlings, cotyledons, leavesand roots were differentiated by organ-specific expressed genes.
In one of these mutants, apm1, the peroxisomes are long and reduced in number, apparently as a result of inhibition of division. We showed that APM1 encodes DRP3A (dynamin-related protein 3A), and that mutations in APM1/DRP3A also caused aberrant morphology of mitochondria. The transient expression analysis showed that DRP3A is associated with the cytosolicsideofperoxisomes. Thesesfindingsindicate that the same dynamin molecule is involved in peroxisomal and mitochondrialdivision in higherplants.
From analyses of apm2 and apm4 mutants which are difectiveinproteintransportbyPTS1-dependent pathway, we determined that APM2 and APM4 genes encode PEROXIN13 (PEX13) and PEX12, respectively, and revealed that they are responsible for PTS2-as well as PTS1-dependent protein on the peroxisomal membrane.
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