2001 Fiscal Year Final Research Report Summary
Study of DNA repair deficient mice
| Project/Area Number |
10044231
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
環境影響評価(含放射線生物学)
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| Research Institution | Tohoku University |
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Principal Investigator |
YASUI Akira Tohoku University, Institute of Development, Aging and Cancer, Department of Molecular Genetics, Professor, 加齢医学研究所, 教授 (60191110)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAO Masashi Tohoku University, Institute of Development, Aging and Cancer, Department of Molecular Genetics, Assistant Professor, 加齢医学研究所, 助手 (70216612)
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| Project Period (FY) |
1998 – 2000
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| Keywords | DNA repair / gene targeting / repair deficient mouse / circadian rhythm / photo repair |
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| Research Abstract |
We isolated two mouse homologues of photolyase gene (mCry1 and mCry2), which encode proteins in the family of blue-light receptors. To explore the biological function of mammalian Cry1 and Cry2, we have generated cry1 and cry2 mutant mice through gene targeting in embryonic stem cells. Since these mutant mice are completely healthy and showed no overt phenotype, we analyzed the possible role for CRY proteins in the biological clock by measuring the circadian wheel-running behavior of cry-knockout mice under normal light/dark (LD) cycles and in constant darkness (DD). Since CRY proteins are able to function as blue-light receptor, these protein may be involved in the light entrainment ability. We found that mice lacking the Cry1 or Cry2 protein display accelerated and delayed free-running (DD) periodicity of locomotor activity, respectively. These findings suggest that Cry1 and Cry2 antagonistically modulate the period length of the clock. Above results indicate, however, that a deficiency in either gene does not produce a detectable loss of light entrainment of locomotor activity. Since cry1 mouse still contain a functional Cry2 protein, we generated double-mutant animals. To our surprise, in the absence of both proteins, an instantaneous and complete loss of free-running rhythmicity is observed. This suggests that, in addition to a possible photoreceptor and antagonistic clock-adjusting function, both proteins are essential for the maintenance of circadian rhytjmicity.
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Research Products
(12 results)
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[Publications] Chigansas, V., Miyaji, E.N., Muotri, A.R., Jacysyn, J.F., Amarante-Mendes, G.P., Yasui, A., and Menck, C.F.M.: "Photorepair prevents UV-induced apoptosis in human cells expressing the marsupial photolyase gene."Cancer Res.. 60. 2458-2463 (2000)
Description
「研究成果報告書概要(欧文)」より
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[Publications] Yagita, K., Yamaguchi, S., Tamanini, F., van der Horst, G.T., Hoeijmakers, J.H., Yasui, A., Loros, J.J., Dunlap, J.C., and Okamura, H.: "Dimerization and nuclear entry of mPER proteins in mammalian cells."Genes Dev.. 14. 1353-1363 (2000)
Description
「研究成果報告書概要(欧文)」より
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[Publications] Okamura, H., Miyake, S., Sumi, Y., Yamaguchi, S., Yasui, A., Muijtjens, M., Hoeijmakers, J.H.J., van der Horst, G.T.J.: "Photic induction of mPer1 and mPer2 in Crydeficient mice lacking a biological clock."Science. 286. 2531-2534 (1999)
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「研究成果報告書概要(欧文)」より
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[Publications] van der Horst, G.T.J., Muijtjens, M., Kobayashi, K., Takano, R., Kanno, S., Takao, M., de Wit, J., Verkerk, A., Eker, A.P.M., van Leenen, D., Buijs, R., Bootsma, D., Hoeijmakers J.H.J., and Yasui A.: "Mammalian Cry1 and Cry2 are essential for maintenance of circadian rhythms."Nature. 398. 627-630 (1999)
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「研究成果報告書概要(欧文)」より
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[Publications] Okano, S., Kanno, S., Takao, M., Eker, A P.M., Isono, K., Tsukahara, Y., and Yasui, A.: "A putative blue-light receptor from Drosophila melanogaster."Photochem. Photobiol.. 69. 108-113 (1999)
Description
「研究成果報告書概要(欧文)」より
