| Project/Area Number |
04454611
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
分子遺伝学・分子生理学
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
WADA Chieko (1993) Virus Research, Kyoto University, Instructor, ウィルス研究所, 助手 (10175698)
由良 隆 (1992) 京都大学, ウイルス研究所, 教授 (20027311)
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| Co-Investigator(Kenkyū-buntansha) |
MORI Hirotada Advanced Institute of Science and Technology, Nara, Associate Professor, 遺伝子教育研究センター, 助教授 (90182203)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥6,700,000 (Direct Cost: ¥6,700,000)
Fiscal Year 1993: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1992: ¥6,100,000 (Direct Cost: ¥6,100,000)
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| Keywords | Heat shock Response / sigma^<32> stabilization / sigma^<32> translational regulation / Heat shock protein / σ^<32> / σ^<32>mRNA高次構造 / 遺伝子発現 / ストレス応答 / 大腸菌 / 熱ショック蛋白貭 / 翻訳制御 / メッセンジャーRNA / σ因子 |
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| Research Abstract |
The well-coordinated cellular response to the environmental stresses is essential for survival and maintenance of healthy life. Our understanding of the molecular regulatory mechanism of heat-shock response has been advanced by recent active investigations, among which studies with Escherichia coli has playd a role of providing basic and leading contributions. A heat-shock treatment triggers an increase of the cellular concentration of an RNA polymerase subunit sigma^<32>, which them induces expression(by transcription)of a group of genes coding for so-called heat-shock proteins such as the molecular chaperones GroE, DnaJ, DnaK, GrpE, and so on.
Our recent ayalysis about the increase of the sigma^<32> concentration revealed that accmulation of abnormal proteins led the otherwise unstable sigma^<32> to become stable. It, however, did not increase the rate of sigma^<32> synthesis. Our results imply that there are at least two distinct pathways for the increase of sigma^<32> concentration. One is the stabilization pathway through accumulation of abnormal proteins, and the other is a pathway for stimulating sigma^<32> synthesis.
For the latter pathway, we have shown the participation of the secondary structure mRNA transcribed from the rpoH gene encoding sigma^<32>. We suspect that there are in addition trans-acting factors ; thus we are engaged in finding them by devising a mutant-selection method.
For the former pathway, we are analysing the domain structure of sigma^<32> by a site-directed-mutagenesis technique to determine the regulatory mechanism for the sigma^<32> stabilization.
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