Department of Biological Sciences and Engineering, Indian Institute of Technology Gandhinagar, Gandhinagar, India.
Department of Biopharmacy, Medical University of Lublin, Lublin, Poland.
BMC Genom Data. 2024 Nov 18;25(1):98. doi: 10.1186/s12863-024-01282-2.
CGGBP1 is a GC-rich DNA-binding protein which is important for genomic integrity, gene expression and epigenome maintenance through regulation of CTCF occupancy and cytosine methylation. It has remained unclear how CGGBP1 integrates multiple diverse functions with its simple architecture of only a DNA-binding domain tethered to a C-terminal tail with low structural rigidity. We have used truncated forms of CGGBP1 with or without the DNA-binding domain (DBD) to assay cytosine methylation and global gene expression. Proximal promoters of CGGBP1-repressed genes, although significantly GC-poor, contain GC-rich transcription factor binding motifs and exhibit base compositions indicative of low C-T transition rates due to prevention of cytosine methylation. Genome-wide analyses of cytosine methylation and binding of CGGBP1 DBD show that CGGBP1 restricts cytosine methylation in a manner that depends on its DBD and its DNA-binding. The CGGBP1-repressed genes show an increase in promoter cytosine methylation alongside a decrease in transcript abundance when the DBD-deficient CGGBP1 is expressed. Our findings suggest that CGGBP1 protects transcription factor binding sites (TFBS) from cytosine methylation-associated loss and thereby regulates gene expression. By analysing orthologous promoter sequences we show that restriction of cytosine methylation is a function of CGGBP1 progressively acquired during vertebrate evolution. A superimposition of our results and evolution of CGGBP1 suggests that mitigation of cytosine methylation is majorly achieved by its N-terminal DBD. Our results position CGGBP1 DNA-binding as a major evolutionarily acquired mechanism through which it keeps cytosine methylation under check and regulates TFBS retention and gene activity.
CGGBP1 是一种富含 GC 的 DNA 结合蛋白,通过调节 CTCF 占据和胞嘧啶甲基化,对基因组完整性、基因表达和表观基因组维持至关重要。目前尚不清楚 CGGBP1 如何将其简单的 DNA 结合结构域与低结构刚性的 C 端尾部连接起来,与多种不同的功能整合在一起。我们使用截短形式的 CGGBP1 及其带有或不带有 DNA 结合域(DBD)的形式来检测胞嘧啶甲基化和全基因表达。CGGBP1 抑制基因的近端启动子,尽管明显 GC 含量低,但含有富含 GC 的转录因子结合基序,并表现出低 C-T 转换率的碱基组成,这是由于阻止了胞嘧啶甲基化。CGGBP1 DBD 的全基因组胞嘧啶甲基化和结合分析表明,CGGBP1 以依赖于其 DBD 和 DNA 结合的方式限制胞嘧啶甲基化。当表达缺乏 DBD 的 CGGBP1 时,CGGBP1 抑制的基因表现出启动子胞嘧啶甲基化增加,同时转录物丰度降低。我们的发现表明,CGGBP1 保护转录因子结合位点(TFBS)免受与胞嘧啶甲基化相关的丢失,从而调节基因表达。通过分析同源启动子序列,我们表明限制胞嘧啶甲基化是 CGGBP1 在脊椎动物进化过程中逐渐获得的功能。我们的结果和 CGGBP1 的进化叠加表明,减轻胞嘧啶甲基化主要是通过其 N 端 DBD 实现的。我们的结果将 CGGBP1 的 DNA 结合定位为一种主要的进化获得机制,通过该机制,它使胞嘧啶甲基化保持在检查之下,并调节 TFBS 保留和基因活性。