CGGBP1 调控 CTCF 结合基序处的胞嘧啶甲基化以抵抗随机性。
CGGBP1-regulated cytosine methylation at CTCF-binding motifs resists stochasticity.
机构信息
HoMeCell Lab, Biological Engineering, Indian Institute of Technology Gandhinagar, Palaj, Gandhinagar, 382355, Gujarat, India.
出版信息
BMC Genet. 2020 Jul 29;21(1):84. doi: 10.1186/s12863-020-00894-8.
BACKGROUND
The human CGGBP1 binds to GC-rich regions and interspersed repeats, maintains homeostasis of stochastic cytosine methylation and determines DNA-binding of CTCF. Interdependence between regulation of cytosine methylation and CTCF occupancy by CGGBP1 remains unknown.
RESULTS
By analyzing methylated DNA-sequencing data obtained from CGGBP1-depleted cells, we report that some transcription factor-binding sites, including CTCF, resist stochastic changes in cytosine methylation. By analysing CTCF-binding sites we show that cytosine methylation changes at CTCF motifs caused by CGGBP1 depletion resist stochastic changes. These CTCF-binding sites are positioned at locations where the spread of cytosine methylation in cis depends on the levels of CGGBP1.
CONCLUSION
Our findings suggest that CTCF occupancy and functions are determined by CGGBP1-regulated cytosine methylation patterns.
背景
人类 CGGBP1 与富含 GC 的区域和散布重复序列结合，维持随机胞嘧啶甲基化的内稳态，并决定 CTCF 的 DNA 结合。CGGBP1 对胞嘧啶甲基化和 CTCF 占有率的调节之间的相互依赖关系尚不清楚。
结果
通过分析从 CGGBP1 耗尽的细胞中获得的甲基化 DNA 测序数据，我们报告说，一些转录因子结合位点，包括 CTCF，抵抗胞嘧啶甲基化的随机变化。通过分析 CTCF 结合位点，我们表明 CGGBP1 耗尽引起的 CTCF 基序中的胞嘧啶甲基化变化抵抗随机变化。这些 CTCF 结合位点位于 cis 中胞嘧啶甲基化扩展依赖 CGGBP1 水平的位置。
结论
我们的发现表明，CTCF 的占有率和功能由 CGGBP1 调节的胞嘧啶甲基化模式决定。
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