CGGBP1-regulated cytosine methylation at CTCF-binding motifs resists stochasticity.

IF 2.9 Q2 Biochemistry, Genetics and Molecular Biology BMC Genetics Pub Date : 2020-07-29 DOI:10.1186/s12863-020-00894-8
Manthan Patel, Divyesh Patel, Subhamoy Datta, Umashankar Singh
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引用次数: 5

Abstract

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.

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cggbp1调节ctcf结合基序上的胞嘧啶甲基化抵抗随机性。
背景:人类CGGBP1结合gc -富区和散布的重复序列,维持随机胞嘧啶甲基化的稳态,并决定CTCF的dna结合。胞嘧啶甲基化调控与CGGBP1占用CTCF之间的相互依存关系尚不清楚。结果:通过分析从cggbp1缺失的细胞中获得的甲基化dna测序数据,我们报告了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,我们发现CGGBP1耗散引起的CTCF基序上胞嘧啶甲基化变化抵抗随机变化。这些ctcf结合位点位于顺式胞嘧啶甲基化的扩散取决于CGGBP1水平的位置。结论:cggbp1调控的胞嘧啶甲基化模式决定了CTCF的占据和功能。
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来源期刊
BMC Genetics
BMC Genetics 生物-遗传学
CiteScore
4.30
自引率
0.00%
发文量
77
审稿时长
4-8 weeks
期刊介绍: BMC Genetics is an open access, peer-reviewed journal that considers articles on all aspects of inheritance and variation in individuals and among populations.
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