| Project/Area Number |
13854002
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| Research Category |
Grant-in-Aid for Scientific Research (S)
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| Allocation Type | Single-year Grants |
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| Research Field |
植物生理
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| Research Institution | National Institute to Basic Biology (2004)
Okazaki National Research Institutes (2001-2003) |
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Principal Investigator |
MURATA Norio National Institute for Basic Biology, Division of Cellular Regulation, Professor, 環境適応研究部門, 教授 (90011569)
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| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Iwane University of Tsukuba, Graduate School of Life and Environmental Sciences, Assistant Professor, 大学院・生命環境科学研究科, 講師 (10290909)
三上 浩司 岡崎国立共同研究機構, 基礎生物学研究所, 助教授 (40222319)
西山 佳孝 岡崎国立共同研究機構, 基礎生物学研究所, 助手 (30281588)
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| Project Period (FY) |
2001 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥123,370,000 (Direct Cost: ¥94,900,000、Indirect Cost: ¥28,470,000)
Fiscal Year 2004: ¥30,940,000 (Direct Cost: ¥23,800,000、Indirect Cost: ¥7,140,000)
Fiscal Year 2003: ¥30,940,000 (Direct Cost: ¥23,800,000、Indirect Cost: ¥7,140,000)
Fiscal Year 2002: ¥30,940,000 (Direct Cost: ¥23,800,000、Indirect Cost: ¥7,140,000)
Fiscal Year 2001: ¥30,550,000 (Direct Cost: ¥23,500,000、Indirect Cost: ¥7,050,000)
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| Keywords | Cold sensor / Histidine kinase / DNA super-coiling / Response regulater / Cyanobacterium / Ser / Thr protein kinases / 遺伝子発現 / DNAミクロアレイ / セリン・スレオニン・キナーゼ / DNAマイクロアレイ / 酸化ストレスセンサー / ヒスチジン・キナーゼ / マルチ・ストレス・センサー / 塩センサー / マルチ・チャンネル・センサー / 浸透圧センサー / プロテオーム |
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| Research Abstract |
(1) The cyanobacterium Synechocystis sp. PCC 6803 contains 44 genes for histidine kinases (Hiks) and 42 genes for response regulators (Rres). We individually inactivated all of these signal transducers and generated knockout libraries. By screening these libraries by cold-inducible expression of genes with genome-wide DNA microarrays we identified Hik33 as only one Hik for cold sensing and Rre 26 and Rre 31 as response regulators located downstreem of Hik33 in the cold signal transduction pathway.
(2) We identified Hik33, which we previously identified as a cold sensor, as a component involved in the signal pathways of hyperosmotic, cold, strong-light and oxidative stress. These findings suggest that Hik33 itself is not specific to the individual stress and that the signal transduction pathways which include Hiks and Rres are more complicated than the simple two-component systems which have been established previously. It is very likely that Hik33 cooperates with other factors that give the specificity to individual stress. Identifications of such factors will be an important subject of further study.
(3) We demonstrated possibilities that some Ser/Thr protein kinases are involved in the cold-signal transduction pathway and that DNA supercoiling may directly sense the cold signals.
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