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Figure S3

January 2013

January 2013

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CC BY 4.0

Authors:

Massachusetts Institute of Technology

Jinan University (Guangzhou, China)

Jonathan J Russin

University of Southern California

The University of Arizona

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DNA methylation vs. gene expression using publicly available expression data in meningiomas. The scatter plots with smoothed density for visualizing the relationship of promoter DNA methylation with publicly available gene expression data (see methods) in malignant and benign meningiomas (Figure S3A, S3B). The relationship of promoter differential methylation with differential gene expression was shown in Figure S3C. (TIF)

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DNA Methylation in the Malignant Transformation of Meningiomas

Article

January 2013

Fan Gao · Lingling Shi · Jonathan J Russin · Liyun Zeng · Kai Wang

Article

Freedom of expression in methylated regions

December 2018 · Nature Reviews Molecular Cell Biology

Eytan Zlotorynski

A plant complex comprising SUVH1, SUVH3, DNAJ1 and DNAJ2 counteracts DNA-methylation-mediated silencing of transposon-neighbouring genes.

Data

Full-text available

Supplemental Figure S1

May 2018

Distribution of differentially methylated locus in LA. (A) The numbers of those differentially methylated loci by chromosome in LA. (B) Proportion of differentially methylated loci given by island functional categories (CpG islands, shores, shelf) showing significant change of DNA methylation in LA. (C) Proportion of differentially methylated loci given by gene functional categories (within 200 ... [Show full abstract] or 1,500 bp of a transcription start site (TSS), 5′UTR, 3′UTR, gene body). (D) The numbers of hypermethylated and hypomethylated loci in LA. (E) The numbers of hypermethylated and hypomethylated genes in LA.

Chapter

Fuzzy Approaches for the Analysis CpG Island Methylation Patterns

May 2007

Introduction Methods Biological Significance Conclusions References

Data

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Figure S2

April 2011

Crosstalk between DNA methylation and H3K27me3 in HBEC. A. Gene bodies marked by DNA methylation and H3K27me3 on human chr19 in HBEC. The numbers indicate genes with gene bodies marked by H3K27me3 or DNA methylation or by both marks with at least 20% of gene body length coverage (p<0.001; Chi square test). B. Composite profile of genes with gene bodies marked by H3K27me3 and DNA methylation with ... [Show full abstract] at least 20% of gene body length coverage. Each gene body was divided into 20 bins and the 5 kb upstream of the TSS and 5 kb downstream of the 3′ gene end were divided into 10 bins. The average signal for each single bin is plotted. Both MIRA and UMC signals are enriched within H3K27me3-covered gene bodies indicating partial methylation. C. Representative epigenetic profile of a chr19 region containing H3K27me3-marked genes (boxes) in HBEC. D. DNA methylation level in gene bodies of different epigenetic gene groups, genes marked by H3K27me3 together with DNA methylation, genes marked by H3K9me3 and H3K36me3, and genes marked by DNA methylation together with H3K36me3. The average of signal in each gene body was plotted for each epigenetic group. A gene was considered marked by a specific epigenetic modification if this mark was present along at least 20% of gene body length. Multiple comparison tests show that all three pairs show statistical difference at p<0.001. E. CpG density in gene bodies for genes marked by H3K27me3 and DNA methylation, by H3K9me3 and H3K36me3, and by DNA methylation together with H3K36me3. Average of CpG density for each gene body was plotted for each epigenetic group. Comparison between H3K27me3-MIRA and H3K36me3-H3K9me3 shows statistical difference (p<0.001). Comparison between H3K36me3-MIRA and H3K36me3-H3K9me3 also shows statistical difference (p<0.001). There is no statistical difference between H3K27me3-MIRA and H3K36me3-MIRA (p>0.05). (PDF)