scholarly journals DNA methylation at differentially methylated regions of imprinted genes is resistant to developmental programming by maternal nutrition

Epigenetics ◽  
2012 ◽  
Vol 7 (10) ◽  
pp. 1200-1210 ◽  
Author(s):  
Elena Ivanova ◽  
Jian-Hua Chen ◽  
Anne Segonds-Pichon ◽  
Susan E. Ozanne ◽  
Gavin Kelsey
Keyword(s):  
Dna Methylation ◽  
Maternal Nutrition ◽  
Developmental Programming ◽  
Imprinted Genes ◽  
Differentially Methylated Regions

scholarly journals Genomic imprinting in germ cells: imprints are under control

Reproduction ◽  
2010 ◽  
Vol 140 (3) ◽  
pp. 411-423 ◽  
Author(s):  
Philippe Arnaud
Keyword(s):  
Dna Methylation ◽  
Genomic Imprinting ◽  
Germ Cells ◽  
Imprinted Genes ◽  
Regulatory Sequences ◽  
Sequence Specificity ◽  
Maternal Allele ◽  
Primary Sequence ◽  
Chromatin Configuration

The cis-acting regulatory sequences of imprinted gene loci, called imprinting control regions (ICRs), acquire specific imprint marks in germ cells, including DNA methylation. These epigenetic imprints ensure that imprinted genes are expressed exclusively from either the paternal or the maternal allele in offspring. The last few years have witnessed a rapid increase in studies on how and when ICRs become marked by and subsequently maintain such epigenetic modifications. These novel findings are summarised in this review, which focuses on the germline acquisition of DNA methylation imprints and particularly on the combined role of primary sequence specificity, chromatin configuration, non-histone proteins and transcriptional events.

106 The Effects of Fetal Programming on Offspring Pancreas DNA Methylation

2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 54-55
Author(s):  
Maria L Hoffman
Keyword(s):  
Dna Methylation ◽  
Fetal Programming ◽  
Maternal Nutrition ◽  
Maternal Diet ◽  
Multiple Generations ◽  
Livestock Species ◽  
Maternal Programming ◽  
Genome Bisulfite Sequencing ◽  
The Many ◽  
Methylation Patterns

Abstract It has been well documented that fetal programming, caused by changes to the maternal environment during pregnancy, can impact the overall health and growth of the offspring in livestock and non-livestock species alike. These effects are observed in the F1 offspring as well as across subsequent generations; however, the mechanisms by which this occurs are still poorly understood. Epigenetics is one of the many mechanisms that is hypothesized to have a role in fetal programming and may be mediating the observed effects across multiple generations. It has been demonstrated by others that DNA methylation patterns can be altered by an individuals’ diet and that the pancreas is vulnerable to the effects of fetal programming. Therefore, we evaluated the effects of poor maternal nutrition during gestation on the pancreas tissue of lambs. We have demonstrated that maternal under- or overnutrition during gestation alters the DNA methylation patterns of the offspring pancreas tissue with these effects being diet dependent and sex specific. We have also begun evaluating the effects of maternal diet in murine models using whole-genome bisulfite sequencing to compare species differences and determine if there are any changes conserved across species. This will allow us to focus on a smaller number of critical factors in individuals as they age and across multiple generations in livestock species such as sheep and cattle. From these data we will be able to elucidate the role DNA methylation has in mediating the effects of maternal programming in the pancreas tissue.

scholarly journals DNA methylation-independent growth restriction and altered developmental programming in a mouse model of preconception male alcohol exposure

Epigenetics ◽  
2017 ◽  
Vol 12 (10) ◽  
pp. 841-853 ◽  
Author(s):  
Richard C. Chang ◽  
William M. Skiles ◽  
Sarah S. Chronister ◽  
Haiqing Wang ◽  
Gabrielle I. Sutton ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Mouse Model ◽  
Alcohol Exposure ◽  
Developmental Programming ◽  
Growth Restriction

scholarly journals Maternal Nutrition Induces Pervasive Gene Expression Changes but No Detectable DNA Methylation Differences in the Liver of Adult Offspring

PLoS ONE ◽  
2014 ◽  
Vol 9 (3) ◽  
pp. e90335 ◽  
Author(s):  
Matthew V. Cannon ◽  
David A. Buchner ◽  
James Hester ◽  
Hadley Miller ◽  
Ephraim Sehayek ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Maternal Nutrition ◽  
Adult Offspring

scholarly journals ZFP57 dictates allelic expression switch of target imprinted genes

2021 ◽  
Vol 118 (5) ◽  
pp. e2005377118
Author(s):  
Weijun Jiang ◽  
Jiajia Shi ◽  
Jingjie Zhao ◽  
Qiu Wang ◽  
Dan Cong ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Notch Signaling ◽  
Notch Pathway ◽  
Notch Signaling Pathway ◽  
Mouse Embryos ◽  
The Other ◽  
Allelic Expression ◽  
Monoallelic Expression ◽  
Imprinted Genes ◽  
Parent Of Origin

ZFP57 is a master regulator of genomic imprinting. It has both maternal and zygotic functions that are partially redundant in maintaining DNA methylation at some imprinting control regions (ICRs). In this study, we found that DNA methylation was lost at most known ICRs in Zfp57 mutant embryos. Furthermore, loss of ZFP57 caused loss of parent-of-origin–dependent monoallelic expression of the target imprinted genes. The allelic expression switch occurred in the ZFP57 target imprinted genes upon loss of differential DNA methylation at the ICRs in Zfp57 mutant embryos. Specifically, upon loss of ZFP57, the alleles of the imprinted genes located on the same chromosome with the originally methylated ICR switched their expression to mimic their counterparts on the other chromosome with unmethylated ICR. Consistent with our previous study, ZFP57 could regulate the NOTCH signaling pathway in mouse embryos by impacting allelic expression of a few regulators in the NOTCH pathway. In addition, the imprinted Dlk1 gene that has been implicated in the NOTCH pathway was significantly down-regulated in Zfp57 mutant embryos. Our allelic expression switch models apply to the examined target imprinted genes controlled by either maternally or paternally methylated ICRs. Our results support the view that ZFP57 controls imprinted expression of its target imprinted genes primarily through maintaining differential DNA methylation at the ICRs.

scholarly journals Placentas from pregnancies conceived by IVF/ICSI have a reduced DNA methylation level at the H19 and MEST differentially methylated regions†

2013 ◽  
Vol 28 (4) ◽  
pp. 1117-1126 ◽  
Author(s):  
Ewka C.M. Nelissen ◽  
John C.M. Dumoulin ◽  
Antoine Daunay ◽  
Johannes L.H. Evers ◽  
Jörg Tost ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Methylation Level ◽  
Differentially Methylated Regions

scholarly journals The H19 Differentially Methylated Region Marks the Parental Origin of a Heterologous Locus without Gametic DNA Methylation

2004 ◽  
Vol 24 (9) ◽  
pp. 3588-3595 ◽  
Author(s):  
Kye-Yoon Park ◽  
Elizabeth A. Sellars ◽  
Alexander Grinberg ◽  
Sing-Ping Huang ◽  
Karl Pfeifer
Keyword(s):  
Dna Methylation ◽  
Mouse Chromosome ◽  
Germ Line ◽  
Transcriptional Silencing ◽  
Chromosome 7 ◽  
Differentially Methylated Region ◽  
Parental Origin ◽  
Imprinted Genes ◽  
Chromosome 5 ◽  
The Third

ABSTRACT Igf2 and H19 are coordinately regulated imprinted genes physically linked on the distal end of mouse chromosome 7. Genetic analyses demonstrate that the differentially methylated region (DMR) upstream of the H19 gene is necessary for three distinct functions: transcriptional insulation of the maternal Igf2 allele, transcriptional silencing of paternal H19 allele, and marking of the parental origin of the two chromosomes. To test the sufficiency of the DMR for the third function, we inserted DMR at two heterologous positions in the genome, downstream of H19 and at the alpha-fetoprotein locus on chromosome 5. Our results demonstrate that the DMR alone is sufficient to act as a mark of parental origin. Moreover, this activity is not dependent on germ line differences in DMR methylation. Thus, the DMR can mark its parental origin by a mechanism independent of its own DNA methylation.

Reproducibility-optimized detection of differential DNA methylation

Epigenomics ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 747-755
Author(s):  
Veronika Suni ◽  
Fatemeh Seyednasrollah ◽  
Bishwa Ghimire ◽  
Sini Junttila ◽  
Asta Laiho ◽  
...  
Keyword(s):  
Dna Methylation ◽  
High Throughput Sequencing ◽  
State Of The Art ◽  
Methylation Status ◽  
Real Data ◽  
Epigenetic Mechanism ◽  
Methylation Analysis ◽  
Test Statistic ◽  
Differentially Methylated Regions ◽  
Dna Methylation Analysis

Aim: DNA methylation is a key epigenetic mechanism regulating gene expression. Identifying differentially methylated regions is integral to DNA methylation analysis and there is a need for robust tools reliably detecting regions with significant differences in their methylation status. Materials & methods: We present here a reproducibility-optimized test statistic (ROTS) for detection of differential DNA methylation from high-throughput sequencing or array-based data. Results: Using both simulated and real data, we demonstrate the ability of ROTS to identify differential methylation between sample groups. Conclusion: Compared with state-of-the-art methods, ROTS shows competitive sensitivity and specificity in detecting consistently differentially methylated regions.

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