Whole Genome Methylation Profiling by Immunoprecipitation of Methylated DNA

2012 ◽  
pp. 69-78
Author(s):  
Andrew J. Sharp
Keyword(s):  
Whole Genome ◽  
Methylated Dna ◽  
Genome Methylation ◽  
Methylation Profiling

scholarly journals Whole-genome methylation profiling from PBMCs in acute-exacerbation COPD patients with good and poor responses to corticosteroid treatment

Genomics ◽  
2019 ◽  
Vol 111 (6) ◽  
pp. 1381-1386
Author(s):  
Shih-Wei Lee ◽  
Hwa-Hwan Hwang ◽  
Paul Wei-Che Hsu ◽  
Tzu-Yi Chuang ◽  
Chi-Wei Liu ◽  
...  
Keyword(s):  
Acute Exacerbation ◽  
Corticosteroid Treatment ◽  
Whole Genome ◽  
Copd Patients ◽  
Genome Methylation ◽  
Methylation Profiling

Global DNA Methylation Profiling Demonstrates That Idiopathic Myelofibrosis Is Characterized by a Distinct Epigenetic Signature with Aberrant Methylation Changes in Genes Involved in Inflammation and Hematopoiesis

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 1536-1536 ◽  
Author(s):  
J. Opalinska ◽  
D. Sohal ◽  
R. Thompson ◽  
L. Zhou ◽  
Y. Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Peripheral Blood ◽  
Aberrant Methylation ◽  
Whole Genome ◽  
Gene Promoters ◽  
Idiopathic Myelofibrosis ◽  
Genome Methylation ◽  
Peripheral Blood Leucocytes ◽  
Methylation Profiling

Abstract Chronic idiopathic myelofibrosis (MF) is a clonal hematopoietic disorder that leads to progressive marrow fibrosis and peripheral cytopenias. Very little is known about the role of aberrant DNA methylation in the pathobiology of this disease. Whole genome methylation was analyzed by a recently described novel method, the HELP assay (HpaII tiny fragment Enrichment by Ligation-mediated PCR; Khulan et al, Genome Res. 2006 Aug;16(8)) that uses differential methylation specific restriction digestion by HpaII and MspI followed by amplification, two color labeling and cohybridization to quantitatively determine individual promoter methylation. A whole genome human promoter array (Nimblegen) was used to determine the level of methylation of 25626 gene promoters by calculating HpaII/MspI cut fragment intensity ratio. Peripheral blood leucocytes from 9 patients with IMF were compared to 9 age-matched normal and anemic controls. Gene expression analysis was performed using 37K oligo maskless arrays using cDNA from the same samples. Methylation analysis showed that myelofibrosis samples clustered separately from normal and anemic controls when grouped by unsupervised clustering based on Pearson’s correlation coefficient. On the other hand, global gene expression demonstrated no clear cut differences between myelofibrosis and control samples suggesting that methylation profiling has greater discriminatory power when compared to conventional gene expression profiling. A high correlation (r=0.88–0.96) was observed between whole genome methylation profiles of matched sets of bone marrow and peripheral blood leucocyte samples from selected patients demonstrating that peripheral blood leucocytes can act as a valid surrogates for epigenomic analysis. Further analysis showed that genes aberrantly methylated in all myelofibrosis samples included v-myc, histone 2A, TNF, TNF Receptor1, FGF14 and others. Functional pathway analysis by Ingenuity showed that pathways involved in Inflammation and Cell signaling were the most affected by epigenetic silencing. Most interestingly, a large proportion of gene promoters were also aberrantly hypomethylated. These included genes for chemokine CXCL13, APC, IL-3, STAT2 and others. The pathways most activated by hypomethylation were involved in hematopoiesis and cell growth and proliferation demonstrating the biological validity of our analysis. Thus, our data demonstrates that myelofibrosis is characterized by distinct epigenetic aberrations that are preserved in peripheral blood leucocytes. These can be the basis of future studies on pathogenesis and diagnosis for this disease and lead to translational studies with agents targeting DNA methylation.

Abstract 2781: Novel putative diagnostic methylation biomarkers for prostate cancer identified by whole genome DNA methylation profiling

2016 ◽  
Author(s):  
Arup Ratan Chakraborty ◽  
Erica Hlavin Bell ◽  
Simon Kriste ◽  
Vanessa Drendel ◽  
Joseph McElRoy ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Dna Methylation ◽  
Whole Genome ◽  
Dna Methylation Profiling ◽  
Methylation Profiling

Abstract B04: The use of whole genome methylation scanning to define genes preferentially suppressed in African American Prostate Cancer

2017 ◽  
Author(s):  
Farah Rahmatpanah ◽  
Kathleen McGuire ◽  
Michael Lilly ◽  
Michael McClelland ◽  
Dan Mercola
Keyword(s):  
Prostate Cancer ◽  
African American ◽  
Whole Genome ◽  
Genome Methylation

338. METHYL BINDING DOMAIN PROTEIN (MBD1) IN THE NUCLEUS OF THE MOUSE ZYGOTE

2010 ◽  
Vol 22 (9) ◽  
pp. 138
Author(s):  
Y. Li ◽  
X. L. Jin ◽  
C. O'Neill
Keyword(s):  
Cell Cycle ◽  
Acid Treatment ◽  
Metaphase Chromosomes ◽  
Methylated Dna ◽  
Stage Of Development ◽  
Genome Methylation ◽  
Mouse Zygote ◽  
Domain Protein ◽  
Proxy Measurement ◽  
Current Paradigm

MBD1 is one of five proteins which bind methylated DNA and regulate gene transcription. The binding of these proteins, particularly MBD1, is commonly used as a proxy measurement of global CpG methylation. Since methylation is reported to be highly dynamic during the first cell-cycle, with reported asymmetric global demethylation of the paternal and maternal genomes by the time of syngamy, we were interested to assess the pattern of staining of the MBD1 during this stage of development. A specific antibody to MBD1 was shown by Western analysis to detect in zygotes a protein of predicted mass. Using immunolocalization, however, we found no staining in pronuclei. Brief acid treatment (10min, 4M HCl) followed by immunolabelling revealed strong pronuclear MBD1 staining throughout the maturation of the zygote and on metaphase chromosomes, indicative of epitope masking under normal staining conditions. Upon unmasking by acid treatment zygotes collected fresh from the oviduct did not show consistent differences in MBD1 staining between the maternal or paternal chromosomes or pronuclei, but for those embryos produced by IVF we found more MBD1 staining in the male paternal pronucleus. Brief treatment with trypsin caused a marked loss of MBD1 staining and this treatment increased the extent of staining of 5-methylcytosine. These results show that MBD1 antigen persists on DNA after treatments normally used for the detection of 5-methylcytosine. MBD1 at least partially masks methylcytosine from immunological detection and the results therefore raise the possibility that the reported changes in genome methylation in the zygote are a consequence of the binding of MBD1. If MBD1 binding is truly a proxy for methylation, the persistence of high levels of MBD1 throughout the first cell-cycle questions the current paradigm of global demethylation during zygote maturation.

Oocyte IVM or vitrification significantly impairs DNA methylation patterns in blastocysts as analysed by single-cell whole-genome methylation sequencing

2020 ◽  
Vol 32 (7) ◽  
pp. 676
Author(s):  
Ya-Han Zhao ◽  
Jing-Jing Wang ◽  
Pei-Pei Zhang ◽  
Hai-Sheng Hao ◽  
Yun-Wei Pang ◽  
...  
Keyword(s):  
Single Cell ◽  
Protein Phosphatase ◽  
Poor Quality ◽  
Protein Phosphatase 1 ◽  
Regulatory Subunit ◽  
Whole Genome ◽  
Genome Methylation ◽  
Sequencing Technique ◽  
Methylation Patterns

To explore the mechanisms leading to the poor quality of IVF blastocysts, the single-cell whole-genome methylation sequencing technique was used in this study to analyse the methylation patterns of bovine blastocysts derived from invivo, fresh (IVF) or vitrified (V_IVF) oocytes. Genome methylation levels of blastocysts in the IVF and V_IVF groups were significantly lower than those of the invivo group (P<0.05). In all, 1149 differentially methylated regions (DMRs) were identified between the IVF and invivo groups, 1578 DMRs were identified between the V_IVF and invivo groups and 151 DMRs were identified between the V_IVF and IVF groups. For imprinted genes, methylation levels of insulin-like growth factor 2 receptor (IGF2R) and protein phosphatase 1 regulatory subunit 9A (PPP1R9A) were lower in the IVF and V_IVF groups than in the invivo group, and the methylation level of paternally expressed 3 (PEG3) was lower in the V_IVF group than in the IVF and invivo groups. Genes with DMRs between the IVF and invivo and the V_IVF and IVF groups were primarily enriched in oocyte maturation pathways, whereas DMRs between the V_IVF and invivo groups were enriched in fertilisation and vitrification-vulnerable pathways. The results of this study indicate that differences in the methylation of critical DMRs may contribute to the differences in quality between invitro- and invivo-derived embryos.

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