| Project/Area Number |
11680676
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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 |
Molecular biology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
NAKAI Akira Assistant Professor, Institute for Frontier Medical Sciences, KYOTO UNIVERSITY, 再生医科学研究所, 助手 (60252516)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2000: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1999: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | heat shock response / heat shock factor / development / cell cycle / spermatogenesis / nuclear translocation / ストレス / 熱ショック / 放射線 / 熱ショック蛋白質 / ストレス応答 / 熱ショック遺伝子 / 転写 |
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| Research Abstract |
1) Analysis of the profile of expression of heat shock transcription factors (HSFs) in developing chicken embryos revealed that HSF3 is a dominant factor and HSF2 is developmentally regulated.
2) A novel heat shock factor, HSF4, is expressed mainly in the brain and lung. Its transcriptional activity increased upon stress conditions, suggesting that HSF4 have a role in induction of target genes in response to stress.
3) We found that activation of HSF1 caused apoptosis of spermatocytes. This result suggests that HSF1 is involved in the elimination of germ cells exposed to stress.
4) We found that HSF3 stayed an inactive dimer when its nuclear localization sequence was deleted. This suggest that nuclear localization signal is involved in the activation of HSF3.
5) Surprisingly, HSF1 and HSF3 regulate expression of Hsp90a in normally growing cells. Loss of HSF1 and HSF3 caused reduction of Hsp90a. Subsequently, cell cycle was blocked at G2 phase even at mild heat shock temperature.
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