| Project/Area Number |
23791156
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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 |
Pediatrics
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| Research Institution | University of Yamanashi |
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Principal Investigator |
MIYAKE Kunio 山梨大学, 医学工学総合研究部, 助教 (60550712)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | エピジェネティクス / 遺伝子発現 / レット症候群 / 自閉症 / MeCP2 / DNAメチル化 / 発達障害 / シナプス / ヒストン修飾 |
|---|
| Research Abstract |
Rett syndrome is a neurodevelopmental and autistic disease caused by mutations of Methyl-CpG-binding protein 2 (MECP2) gene. MeCP2 protein binds to methylated gene promoters to suppress their expression, indicating that Rett syndrome is caused by the deregulation of target genes. However, it is likely that there are more unidentified neuronal MeCP2-targets associated with the neurological features of RTT. Using a genome-microarray approach, we found 22 genomic regionsthat contain sites potentially regulated by MeCP2. Within these regions, Chromatinimmunoprecipitation (ChIP) analysis revealed that MeCP2 binds to the upstream regions of the LIN7A, PCDHB1 and PCDH7. Since these genes are generally essential for brain development, aberrant regulation of these molecules may contribute to the pathogenesis of the neurological features observed in Rett syndrome.
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