| Budget Amount *help |
¥20,670,000 (Direct Cost: ¥15,900,000、Indirect Cost: ¥4,770,000)
Fiscal Year 2013: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2012: ¥8,450,000 (Direct Cost: ¥6,500,000、Indirect Cost: ¥1,950,000)
Fiscal Year 2011: ¥9,230,000 (Direct Cost: ¥7,100,000、Indirect Cost: ¥2,130,000)
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| Research Abstract |
It is well known that DNA methylation and histone methylation suppress transcription of retrotransposons. In mouse embryonic stem cells (ESCs), histone H3 lysine 9 methylation (H3K9me) plays crucial roles for repression of endogenous retroviruses (ERVs), some of which are still active for transposition. Although human ERVs (HERVs) are not active for transposition, many of them are still transcriptionally active and reactivation of HERVs is linked with cell type specific gene expression or tumorigenesis. To elucidate how histone methylation including H3K9me is crucial for repression of HERVs, we tried to establish human iPS/ES cells deficient for H3K9 methyltransferase SETDB1. Using the CRISPR/Cas9 and guide RNA system, we confirmed that SETDB1 can be disrupted by the system. Once we obtain conditional SETDB1 KO human iPS cells, we would like to analyze how transcription of HERVs is regulated by SETDB1 and how SETDB1 is crucial for silencing of other types of retrotransposons in human.
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