| Budget Amount *help |
¥17,290,000 (Direct Cost: ¥13,300,000、Indirect Cost: ¥3,990,000)
Fiscal Year 2023: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2022: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2021: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2020: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2019: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
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| Outline of Final Research Achievements |
Using iPS cells derived from CHARGE syndrome patients, the research involved brain organoid models to investigate the epigenomic regulatory mechanisms of CHD7's target genes. Methods included histological examination and single-cell level RNA-Seq analyses to explore the target genes and epigenomic states influenced by CHD7. The study found that CHD7 binds with tissue-specific pioneer factors to regulate enhancer activation and identified abnormalities in glial cell maturation. Additionally, a novel factor, Factor X, was discovered to interact with CHD7, forming droplets in the nucleus, particularly in neural progenitor cells, concentrating transcriptional activators and positively regulating CHD7 activity. Inhibition of this droplet formation in Factor X resulted in phenotypes similar to those of CHARGE syndrome patients' iPS cells, suggesting new mechanisms in CHD7 function.
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