We are analyzing https://link.springer.com/article/10.1186/1471-2164-15-119.

Title:
Effects of cytosine methylation on transcription factor binding sites | BMC Genomics
Description:
Background DNA methylation in promoters is closely linked to downstream gene repression. However, whether DNA methylation is a cause or a consequence of gene repression remains an open question. If it is a cause, then DNA methylation may affect the affinity of transcription factors (TFs) for their binding sites (TFBSs). If it is a consequence, then gene repression caused by chromatin modification may be stabilized by DNA methylation. Until now, these two possibilities have been supported only by non-systematic evidence and they have not been tested on a wide range of TFs. An average promoter methylation is usually used in studies, whereas recent results suggested that methylation of individual cytosines can also be important. Results We found that the methylation profiles of 16.6% of cytosines and the expression profiles of neighboring transcriptional start sites (TSSs) were significantly negatively correlated. We called the CpGs corresponding to such cytosines “traffic lights”. We observed a strong selection against CpG “traffic lights” within TFBSs. The negative selection was stronger for transcriptional repressors as compared with transcriptional activators or multifunctional TFs as well as for core TFBS positions as compared with flanking TFBS positions. Conclusions Our results indicate that direct and selective methylation of certain TFBS that prevents TF binding is restricted to special cases and cannot be considered as a general regulatory mechanism of transcription.
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Keywords {🔍}

methylation, pubmed, dna, article, google, scholar, cpg, cas, tfbss, binding, traffic, gene, cytosines, tfs, lights, transcription, central, expression, cell, tfbs, positions, scc, cytosine, sites, number, methylated, information, additional, data, types, file, promoters, promoter, overlapping, regulation, science, analysis, regions, positive, results, human, nature, genet, content, profiles, study, significant, genome, predicted, nat,

Topics {✒️}

conventional view bi-modal dna-binding protein author information authors open access article cell-type-specific regulatory patterns timo lassmann alistair rr forrest computational systems biology dna-binding factors shape dynamic dna methylation/de-methylation widespread site-dependent buffering methyl-cpg binding protein article download pdf author correspondence methylation-dependent transcription regulation reported cage-tag clusters dnmt1-deficient mouse embryos profile dna methylation riken preventive medicine understanding beta-cell dysfunction hideya kawaji methylation/expression profile half-cre sequences creates genome-wide dna methylation sequence-specific consensus normalized methylated profile evaluate genome-wide expression transcription factor yy1 n-myc target genes cpg affects transcription related subjects genome-wide dna hydroxymethylation cell-specific tf binding 𝑀 𝑎 chip-seq peak data chip-seq peak regions cage-tag clusters cage-tag cluster transcription-regulating factors induce histone deacetylation pwm-based method generated full size image tissue-specific genes rrbs technique measures computational facilities provided identify transcription factors affect transcriptional regulation methylation profile methylation-dependent regulation single cpg site

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         headline:Effects of cytosine methylation on transcription factor binding sites
         description:DNA methylation in promoters is closely linked to downstream gene repression. However, whether DNA methylation is a cause or a consequence of gene repression remains an open question. If it is a cause, then DNA methylation may affect the affinity of transcription factors (TFs) for their binding sites (TFBSs). If it is a consequence, then gene repression caused by chromatin modification may be stabilized by DNA methylation. Until now, these two possibilities have been supported only by non-systematic evidence and they have not been tested on a wide range of TFs. An average promoter methylation is usually used in studies, whereas recent results suggested that methylation of individual cytosines can also be important. We found that the methylation profiles of 16.6% of cytosines and the expression profiles of neighboring transcriptional start sites (TSSs) were significantly negatively correlated. We called the CpGs corresponding to such cytosines “traffic lights”. We observed a strong selection against CpG “traffic lights” within TFBSs. The negative selection was stronger for transcriptional repressors as compared with transcriptional activators or multifunctional TFs as well as for core TFBS positions as compared with flanking TFBS positions. Our results indicate that direct and selective methylation of certain TFBS that prevents TF binding is restricted to special cases and cannot be considered as a general regulatory mechanism of transcription.
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            Transcription factor binding sites
            Transcriptional regulation
            CAGE
            RRBS
            CpG “traffic lights”
            Bioinformatics
            Computational biology
            Life Sciences
            general
            Microarrays
            Proteomics
            Animal Genetics and Genomics
            Microbial Genetics and Genomics
            Plant Genetics and Genomics
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      headline:Effects of cytosine methylation on transcription factor binding sites
      description:DNA methylation in promoters is closely linked to downstream gene repression. However, whether DNA methylation is a cause or a consequence of gene repression remains an open question. If it is a cause, then DNA methylation may affect the affinity of transcription factors (TFs) for their binding sites (TFBSs). If it is a consequence, then gene repression caused by chromatin modification may be stabilized by DNA methylation. Until now, these two possibilities have been supported only by non-systematic evidence and they have not been tested on a wide range of TFs. An average promoter methylation is usually used in studies, whereas recent results suggested that methylation of individual cytosines can also be important. We found that the methylation profiles of 16.6% of cytosines and the expression profiles of neighboring transcriptional start sites (TSSs) were significantly negatively correlated. We called the CpGs corresponding to such cytosines “traffic lights”. We observed a strong selection against CpG “traffic lights” within TFBSs. The negative selection was stronger for transcriptional repressors as compared with transcriptional activators or multifunctional TFs as well as for core TFBS positions as compared with flanking TFBS positions. Our results indicate that direct and selective methylation of certain TFBS that prevents TF binding is restricted to special cases and cannot be considered as a general regulatory mechanism of transcription.
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         Transcription factor binding sites
         Transcriptional regulation
         CAGE
         RRBS
         CpG “traffic lights”
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         Computational biology
         Life Sciences
         general
         Microarrays
         Proteomics
         Animal Genetics and Genomics
         Microbial Genetics and Genomics
         Plant Genetics and Genomics
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      name:Laboratory of Bioinformatics and Systems Biology, Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia
      name:Department of Computational Systems Biology, Vavilov Institute of General Genetics, Russian Academy of Sciences, Moscow, Russia
      name:Computational Bioscience Research Center, Computer, Electrical and Mathematical Sciences and Engineering Division, King Abdullah University of Science and Technology (KAUST), Thuwal, Saudi Arabia
      name:Computational Bioscience Research Center, Computer, Electrical and Mathematical Sciences and Engineering Division, King Abdullah University of Science and Technology (KAUST), Thuwal, Saudi Arabia
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      name:RIKEN Preventive Medicine and Diagnosis Innovation Program, Wako, Japan
      name:RIKEN Omics Science Center, Yokohama, Japan
      name:RIKEN Center for Life Science Technologies, Division of Genomic Technologies, Yokohama, Japan
      name:RIKEN Omics Science Center, Yokohama, Japan
      name:RIKEN Omics Science Center, Yokohama, Japan
      name:RIKEN Center for Life Science Technologies, Division of Genomic Technologies, Yokohama, Japan
      name:Computational Bioscience Research Center, Computer, Electrical and Mathematical Sciences and Engineering Division, King Abdullah University of Science and Technology (KAUST), Thuwal, Saudi Arabia

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