| Budget Amount *help |
¥77,870,000 (Direct Cost: ¥59,900,000、Indirect Cost: ¥17,970,000)
Fiscal Year 2014: ¥14,560,000 (Direct Cost: ¥11,200,000、Indirect Cost: ¥3,360,000)
Fiscal Year 2013: ¥15,210,000 (Direct Cost: ¥11,700,000、Indirect Cost: ¥3,510,000)
Fiscal Year 2012: ¥15,990,000 (Direct Cost: ¥12,300,000、Indirect Cost: ¥3,690,000)
Fiscal Year 2011: ¥15,860,000 (Direct Cost: ¥12,200,000、Indirect Cost: ¥3,660,000)
Fiscal Year 2010: ¥16,250,000 (Direct Cost: ¥12,500,000、Indirect Cost: ¥3,750,000)
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| Outline of Final Research Achievements |
Histone H3 di/trimethylation at lysine 36 (H3K36me2/3) is associated with actively transcribed regions, however, the control mechanisms and functions of H3K36me in higher eukaryotes are still enigmatic.
We found that H3K36 methyltransferase Wolf-Hirschhorn syndrome candidate 1 (WHSC1) associates with not only transcription factors but also DNA-damage response factors without exogenous DNA-damage, suggesting molecular coupling between transcription and DNA repair. Non-competitive reconstitution of hematopoietic cell analysis reveals that Whsc1 is required for normal B-cell development in vivo. The absence of Whsc1 partially blocks V(D)J recombination and induces apoptosis during early B-cell development. p53-deficiency rescues abnormal B-cell differentiation from Whsc1-/- hematopoietic stem cells. Based on these results we propose that Whsc1 links transcription and DNA damage repair for maintenance of genome integrity.
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