| Project/Area Number |
17590429
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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 |
Virology
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| Research Institution | Aichi Cancer Center Research Institute |
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Principal Investigator |
ISOMURA Hiroki Department of Virology, Aichi Cancer Center Research Institute, Senior Researcher, 腫瘍ウイルス学部, 主任研究員 (20294415)
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| Co-Investigator(Kenkyū-buntansha) |
大黒 徹 愛知県がんセンター(研究所), 腫瘍ウイルス学部, 主任研究員 (80291409)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2006: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2005: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Cytomegalovirus / Transcriptional regulation / 遺伝子制御 / ヒトサイトメガロウイルス / エンハンサー / Sp1 / 前初期遺伝子 / BAC |
|---|
| Research Abstract |
We previous demonstrated that the major immediate early (MIE) proximal enhancer containing one GC box and the TATA box containing promoter are minimal elements required for transcription and viral replication (H.Isomura et al. J.Virol. 78:12788, 2004). Here we report that Electrophoretic mobility shift assays (EMSAs) detected binding of Sp1 and Sp3 transcription factors to the GC boxes located at approximately-55 and -75 relative to the transcription start site (+1). Reporter gene experiments showed that both of the Sp1/Sp3 binding sites have a positive and synergistic effect on the HCMV MIE promoter. After infection, the level of Sp1 increased while Sp3 remain constant. There was little to no change in MIE transcription or viral replication for recombinant viruses with one or the other Sp1/Sp3 binding site mutated. In contrast, mutation of both Sp1/Sp3 binding sites caused inefficient MIE transcription and viral replication. These data indicate that the Sp1/3 binding sites have a significant role in HCMV replication.
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