| Project/Area Number |
24790436
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Virology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
YAMAGISHI Makoto 東京大学, 新領域創成科学研究科, 特任研究員 (90625261)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | エピジェネティクス / HIV-1 / HTLV-1 / 潜伏化 / ATL / ウイルス / 遺伝子 / シグナル伝達 / miRNA |
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| Research Abstract |
The HIV-1 latency remains a principal obstacle in curing AIDS. We revealed a molecular characterization of distinct populations at an early phase of HIV-1 infection. We developed an original dual-color reporter virus to monitor LTR kinetics from establishment to maintenance stage. We found that there are two ways of latency establishment i.e., by immediate silencing and slow inactivation from active infection. Histone covalent modifications, particularly PRC2-mediated H3K27 trimethylation, appeared to dominate viral transcription at the early phase. PRC2 also contributes to time-dependent LTR dormancy.
To view epigenetic landscape in ATL and HTLV-1-infected cells, we performed global histone methylation profiling by high-resolution promoter array. We successfully detected the numerous gene promoters with aberrant repressive H3K27me3 mark in ATL cells. Interestingly, Tax-triggered immortalizing cells partially mimicked the methylation pattern observed in ATL cells.
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