scholarly journals A Genome-Wide Screen for Normally Methylated Human CpG Islands That Can Identify Novel Imprinted Genes

2002 ◽  
Vol 12 (4) ◽  
pp. 543-554 ◽  
Author(s):  
L. Z. Strichman-Almashanu ◽  
R. S. Lee ◽  
P. O. Onyango ◽  
E. Perlman ◽  
F. Flam ◽  
...  
Keyword(s):  
Cpg Islands ◽  
Imprinted Genes ◽  
Genome Wide ◽  
A Genome

scholarly journals A genome-wide approach reveals novel imprinted genes expressed in the human placenta

Epigenetics ◽  
2012 ◽  
Vol 7 (9) ◽  
pp. 1079-1090 ◽  
Author(s):  
Sandrine Barbaux ◽  
Géraldine Gascoin-Lachambre ◽  
Christophe Buffat ◽  
Paul Monnier ◽  
Françoise Mondon ◽  
...  
Keyword(s):  
Human Placenta ◽  
Imprinted Genes ◽  
Genome Wide ◽  
A Genome

scholarly journals DNA methylation of intragenic CpG islands depends on their transcriptional activity during differentiation and disease

2017 ◽  
Vol 114 (36) ◽  
pp. E7526-E7535 ◽  
Author(s):  
Danuta M. Jeziorska ◽  
Robert J. S. Murray ◽  
Marco De Gobbi ◽  
Ricarda Gaentzsch ◽  
David Garrick ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Dna Methyltransferase ◽  
Cpg Islands ◽  
Naturally Occurring ◽  
Genome Wide ◽  
A Genome ◽  
Primary Determinant ◽  
Development And Differentiation ◽  
Intrinsic Capacity

The human genome contains ∼30,000 CpG islands (CGIs). While CGIs associated with promoters nearly always remain unmethylated, many of the ∼9,000 CGIs lying within gene bodies become methylated during development and differentiation. Both promoter and intragenic CGIs may also become abnormally methylated as a result of genome rearrangements and in malignancy. The epigenetic mechanisms by which some CGIs become methylated but others, in the same cell, remain unmethylated in these situations are poorly understood. Analyzing specific loci and using a genome-wide analysis, we show that transcription running across CGIs, associated with specific chromatin modifications, is required for DNA methyltransferase 3B (DNMT3B)-mediated DNA methylation of many naturally occurring intragenic CGIs. Importantly, we also show that a subgroup of intragenic CGIs is not sensitive to this process of transcription-mediated methylation and that this correlates with their individual intrinsic capacity to initiate transcription in vivo. We propose a general model of how transcription could act as a primary determinant of the patterns of CGI methylation in normal development and differentiation, and in human disease.

scholarly journals A Genome-Wide Survey of Imprinted Genes in Rice Seeds Reveals Imprinting Primarily Occurs in the Endosperm

PLoS Genetics ◽  
2011 ◽  
Vol 7 (6) ◽  
pp. e1002125 ◽  
Author(s):  
Ming Luo ◽  
Jennifer M. Taylor ◽  
Andrew Spriggs ◽  
Hongyu Zhang ◽  
Xianjun Wu ◽  
...  
Keyword(s):  
Imprinted Genes ◽  
Genome Wide ◽  
A Genome ◽  
Rice Seeds ◽  
Genome Wide Survey

A genome-wide approach to identifying novel-imprinted genes

2007 ◽  
Vol 122 (6) ◽  
pp. 625-634 ◽  
Author(s):  
Katherine S. Pollard ◽  
David Serre ◽  
Xu Wang ◽  
Heng Tao ◽  
Elin Grundberg ◽  
...  
Keyword(s):  
Imprinted Genes ◽  
Genome Wide ◽  
A Genome

scholarly journals The SAM domain-containing protein 1 (SAMD1) acts as a repressive chromatin regulator at unmethylated CpG islands

2021 ◽  
Vol 7 (20) ◽  
pp. eabf2229
Author(s):  
Bastian Stielow ◽  
Yuqiao Zhou ◽  
Yinghua Cao ◽  
Clara Simon ◽  
Hans-Martin Pogoda ◽  
...  
Keyword(s):  
Transcriptional Repression ◽  
Cpg Islands ◽  
Winged Helix ◽  
Sam Domain ◽  
Genome Wide ◽  
Chromatin Regulator ◽  
A Genome ◽  
Dna Elements ◽  
Regulatory Dna ◽  
Winged Helix Domain

CpG islands (CGIs) are key regulatory DNA elements at most promoters, but how they influence the chromatin status and transcription remains elusive. Here, we identify and characterize SAMD1 (SAM domain-containing protein 1) as an unmethylated CGI-binding protein. SAMD1 has an atypical winged-helix domain that directly recognizes unmethylated CpG-containing DNA via simultaneous interactions with both the major and the minor groove. The SAM domain interacts with L3MBTL3, but it can also homopolymerize into a closed pentameric ring. At a genome-wide level, SAMD1 localizes to H3K4me3-decorated CGIs, where it acts as a repressor. SAMD1 tethers L3MBTL3 to chromatin and interacts with the KDM1A histone demethylase complex to modulate H3K4me2 and H3K4me3 levels at CGIs, thereby providing a mechanism for SAMD1-mediated transcriptional repression. The absence of SAMD1 impairs ES cell differentiation processes, leading to misregulation of key biological pathways. Together, our work establishes SAMD1 as a newly identified chromatin regulator acting at unmethylated CGIs.

scholarly journals Nuclease deficiencies alter plasma cell-free DNA methylation profiles

2021 ◽  
pp. gr.275426.121
Author(s):  
Diana Siao Cheng Han ◽  
Meng Ni ◽  
Rebecca Wing Yan Chan ◽  
Danny Ka Lok Wong ◽  
Linda T Hiraki ◽  
...  
Keyword(s):  
Fragment Size ◽  
Cpg Islands ◽  
Periodic Pattern ◽  
Open Chromatin ◽  
Cell Free Dna ◽  
Free Dna ◽  
Genome Wide ◽  
A Genome ◽  
Wide Scale ◽  
Deficient Mice

The effects of DNASE1L3 or DNASE1 deficiency on cell-free DNA (cfDNA) methylation was explored in plasma of mice deficient in these nucleases and in DNASE1L3-deficient humans. Compared to wild-type cfDNA, cfDNA in Dnase1l3-deficient mice was significantly hypomethylated, while cfDNA in Dnase1-deficient mice was hypermethylated. The cfDNA hypomethylation in Dnase1l3-deficient mice was due to increased fragmentation and representation from open chromatin regions (OCRs) and CpG islands (CGIs). These findings were absent in Dnase1-deficient mice, demonstrating the preference of DNASE1 to cleave in hypomethylated OCRs and CGIs. We also observed a substantial decrease of fragment ends and coverage at methylated CpGs in the absence of DNASE1L3, thereby demonstrating that DNASE1L3 prefers to cleave at methylated CpGs. Furthermore, we found that methylation levels of cfDNA varied by fragment size in a periodic pattern, with cfDNA of specific sizes being more hypomethylated and enriched for OCRs and CGIs. These findings were confirmed in DNASE1L3-deficient human cfDNA. Thus, we have found that nuclease-mediated cfDNA fragmentation markedly affected cfDNA methylation level on a genome-wide scale. This work provides a foundational understanding of the relationship between methylation, nuclease biology and cfDNA fragmentation.

Genome-Wide De Novo Methylation in Epithelial Ovarian Cancer

2011 ◽  
Vol 21 (2) ◽  
pp. 269-279 ◽  
Author(s):  
Rachel Michaelson-Cohen ◽  
Ilana Keshet ◽  
Ravid Straussman ◽  
Merav Hecht ◽  
Howard Cedar ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Differentiation ◽  
Gene Silencing ◽  
De Novo ◽  
Cpg Islands ◽  
Aberrant Methylation ◽  
Genome Wide ◽  
A Genome ◽  
Treatment Responsiveness ◽  
De Novo Methylation

Background:DNA methylation regulates gene expression during development. The methylation pattern is established at the time of implantation. CpG islands are genome regions usually protected from methylation; however, selected islands are methylated later. Many undergo methylation in cancer, causing epigenetic gene silencing. Aberrant methylation occurs early in tumorigenesis, in a specific pattern, inhibiting differentiation.Although methylation of specific genes in ovarian tumors has been demonstrated in numerous studies, they represent only a fraction of all methylated genes in tumorigenesis.Objectives:To explore the hypermethylation design in ovarian cancer compared with the methylation profile of normal ovaries, on a genome-wide scale, thus shedding light on the role of gene silencing in ovarian carcinogenesis.Identifying genes that undergo de novo methylation in ovarian cancer may assist in creating biomarkers for disease diagnosis, prognosis, and treatment responsiveness.Methods:DNA was collected from human epithelial ovarian cancers and normal ovaries. Methylation was detected by immunoprecipitation using 5-methyl-cytosine-antibodies. DNA was hybridized to a CpG island microarray containing 237,220 gene promoter probes. Results were analyzed by hybridization intensity, validated by bisulfite analysis.Results:A total of 367 CpG islands were specifically methylated in cancer cells. There was enrichment of methylated genes in functional categories related to cell differentiation and proliferation inhibition. It seems that their silencing enables tumor proliferation.Conclusions:This study provides new perspectives on methylation in ovarian carcinoma, genome-wide. It illustrates how methylation of CpG islands causes silencing of genes that have a role in cell differentiation and functioning. It creates potential biomarkers for diagnosis, prognosis, and treatment responsiveness.

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