波里斯/CTCFL在表观遗传上重新编程了集群的CTCF结合点,使其成为替代的转录起始点
Elena M Pugacheva1, Dharmendra Nath Bhatt2, Samuel Rivero-Hinojosa3
1Molecular Pathology Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, 20892, USA. epugacheva@niaid.nih.gov.
Genome biology
|January 31, 2024
概括
波里斯/CTCFL蛋白重编程CTCF结合部位变成活跃促进体,驱动癌症和生殖细胞中的基因表达. 这种机制解释了癌症发生和精子发生中的替代促进体激活.
科学领域:
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 分子生物学分子生物学
- 癌症研究 癌症研究
背景情况:
- 替代性促进体在癌症和精子生成中去调节基因表达.
- 替代促进体激活的机制在很大程度上是未知的.
研究的目的:
- 阐明替代癌症和丸特异性转录激活的机制.
主要方法:
- 研究了CTCF结合部位的表观遗传重编程.
- 分析了BORIS/CTCFL在招募染色体重塑因子 (例如SRCAP) 中的作用.
- 评估了基因组变异交换 (H2A到H2A.Z) 和染色质放松.
主要成果:
- 跨基因和内基因CTCF位点在表观遗传上被重新编程为生殖细胞和癌细胞中的活性促进体.
- 博里斯/CTCFL通过招募SRCAP并促进H2A.Z的合并来触发这种重新编程.
- 重编程的CTCF位点驱动癌症丸基因,lncRNA,复原伪基因和可转移元素的表达.
结论:
- 波里斯作为一个转录因子,在表观遗传上重新编程CTCF结合点.
- 这一过程创造了活跃的转录起点,促进了从胚胎和癌细胞中的替代促进体转录.
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