Imprinting on distal chromosome 7 in the placenta involves repressive histone methylation independent of DNA methylation

2004 ◽  
Vol 36 (12) ◽  
pp. 1291-1295 ◽  
Author(s):  
Annabelle Lewis ◽  
Kohzoh Mitsuya ◽  
David Umlauf ◽  
Paul Smith ◽  
Wendy Dean ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Histone Methylation ◽  
Chromosome 7 ◽  
Distal Chromosome

scholarly journals G9a Histone Methyltransferase Contributes to Imprinting in the Mouse Placenta

2007 ◽  
Vol 28 (3) ◽  
pp. 1104-1113 ◽  
Author(s):  
Alexandre Wagschal ◽  
Heidi G. Sutherland ◽  
Kathryn Woodfine ◽  
Amandine Henckel ◽  
Karim Chebli ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Histone Methylation ◽  
Histone Methyltransferase ◽  
Chromosome 7 ◽  
Gene Repression ◽  
Imprinted Genes ◽  
Set Domain ◽  
Imprinted Gene ◽  
Mouse Placenta ◽  
Distal Chromosome

ABSTRACT Whereas DNA methylation is essential for genomic imprinting, the importance of histone methylation in the allelic expression of imprinted genes is unclear. Imprinting control regions (ICRs), however, are marked by histone H3-K9 methylation on their DNA-methylated allele. In the placenta, the paternal silencing along the Kcnq1 domain on distal chromosome 7 also correlates with the presence of H3-K9 methylation, but imprinted repression at these genes is maintained independently of DNA methylation. To explore which histone methyltransferase (HMT) could mediate the allelic H3-K9 methylation on distal chromosome 7, and at ICRs, we generated mouse conceptuses deficient for the SET domain protein G9a. We found that in the embryo and placenta, the differential DNA methylation at ICRs and imprinted genes is maintained in the absence of G9a. Accordingly, in embryos, imprinted gene expression was unchanged at the domains analyzed, in spite of a global loss of H3-K9 dimethylation (H3K9me2). In contrast, the placenta-specific imprinting of genes on distal chromosome 7 is impaired in the absence of G9a, and this correlates with reduced levels of H3K9me2 and H3K9me3. These findings provide the first evidence for the involvement of an HMT and suggest that histone methylation contributes to imprinted gene repression in the trophoblast.

scholarly journals Multiple Mechanisms Regulate Imprinting of the Mouse Distal Chromosome 7 Gene Cluster

1998 ◽  
Vol 18 (6) ◽  
pp. 3466-3474 ◽  
Author(s):  
Tamara Caspary ◽  
Michele A. Cleary ◽  
Catherine C. Baker ◽  
Xiao-Juan Guan ◽  
Shirley M. Tilghman
Keyword(s):  
Dna Methylation ◽  
Gene Cluster ◽  
Genomic Imprinting ◽  
Dna Methyltransferase ◽  
Regulatory Elements ◽  
Chromosome 7 ◽  
Imprinted Genes ◽  
Global Regulator ◽  
Loss Of Imprinting ◽  
Distal Chromosome

ABSTRACT Genomic imprinting is an epigenetic process that results in the preferential silencing of one of the two parental copies of a gene. Although the precise mechanisms by which genomic imprinting occurs are unknown, the tendency of imprinted genes to exist in chromosomal clusters suggests long-range regulation through shared regulatory elements. We characterize a 800-kb region on the distal end of mouse chromosome 7 that contains a cluster of four maternally expressed genes, H19, Mash2, Kvlqt1, andp57Kip2 , as well as two paternally expressed genes, Igf2 and Ins2, and assess the expression and imprinting of Mash2, Kvlqt1, andp57Kip2 during development in embryonic and extraembryonic tissues. Unlike Igf2 and Ins2, which depend on H19 for their imprinting,Mash2, p57Kip2 , andKvlqt1 are unaffected by a deletion of the H19gene region, suggesting that these more telomeric genes are not regulated by the mechanism that controls H19,Igf2, and Ins2. Mutations in humanp57Kip2 have been implicated in Beckwith-Wiedemann syndrome, a disease that has also been associated with loss of imprinting of IGF2. We find, however, that a deletion of the gene has no effect on imprinting within the cluster. Surprisingly, the three maternally expressed genes are regulated very differently by DNA methylation; p57Kip2 is activated, Kvlqt1 is silenced, and Mash2 is unaffected in mice lacking DNA methyltransferase. We conclude thatH19 is not a global regulator of imprinting on distal chromosome 7 and that the telomeric genes are imprinted by a separate mechanism(s).

DNA methyltransferase inhibitors modulate histone methylation: epigenetic crosstalk between H3K4me3 and DNA methylation during sperm differentiation

Zygote ◽  
2021 ◽  
pp. 1-6
Author(s):  
Liliana Burlibaşa ◽  
Alina-Teodora Nicu ◽  
Carmen Domnariu
Keyword(s):  
Dna Methylation ◽  
Histone Methylation ◽  
Dna Methyltransferase ◽  
Integrated Approach ◽  
Regulatory Mechanisms ◽  
Temporal Expression ◽  
Dna Methyltransferase Inhibitors ◽  
Expression Of Genes ◽  
Species Survival ◽  
Advanced Stages

Summary The process of cytodifferentiation in spermatogenesis is governed by a unique genetic and molecular programme. In this context, accurate ‘tuning’ of the regulatory mechanisms involved in germ cells differentiation is required, as any error could have dramatic consequences on species survival and maintenance. To study the processes that govern the spatial–temporal expression of genes, as well as analyse transmission of epigenetic information to descendants, an integrated approach of genetics, biochemistry and cytology data is necessary. As information in the literature on interplay between DNA methylation and histone H3 lysine 4 trimethylation (H3K4me3) in the advanced stages of murine spermatogenesis is still scarce, we investigated the effect of a DNA methyltransferase inhibitor, 5-aza-2′-deoxycytidine, at the cytological level using immunocytochemistry methodology. Our results revealed a particular distribution of H3K4me3 during sperm cell differentiation and highlighted an important role for regulation of DNA methylation in controlling histone methylation and chromatin remodelling during spermatogenesis.

The Emerging Role of Epigenetic Methylation in Kidney Disease

2021 ◽  
Vol 28 ◽  
Author(s):  
Li Wen ◽  
Hong-liu Yang ◽  
Lin Lin ◽  
Liang Ma ◽  
Ping Fu
Keyword(s):  
Dna Methylation ◽  
Kidney Disease ◽  
Histone Methylation ◽  
Kidney Diseases ◽  
Therapeutic Approaches ◽  
Promoter Regions ◽  
Recent Advances ◽  
Epigenetic Methylation

: Kidney disease has complex and multifactorial pathophysiology and pathogenesis. Recent studies have revealed that epigenetic methylation changes, namely DNA methylation, histone methylation and non-histone methylation, are strongly implicated in various forms of kidney diseases. This review provides a perspective on the emerging role of epigenetic methylation in kidney disease, including the effects of DNA methylation in diverse promoter regions, regulation and implication of histone methylation, and recent advances and potential directions related to non-histone methylation. Monitoring or targeting epigenetic methylation has potential to contribute to development of therapeutic approaches for multiple kidney diseases.

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.

Localization of the Mouse Gene (Bc1) Encoding Neural BC1 RNA Near the Fibroblast Growth Factor 3 Locus (Fgf3) on Distal Chromosome 7

Genomics ◽  
1997 ◽  
Vol 44 (1) ◽  
pp. 153-154 ◽  
Author(s):  
Benjamin A. Taylor ◽  
Ann Navin ◽  
Boris V. Skryabin ◽  
Jürgen Brosius
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Mouse Gene ◽  
Chromosome 7 ◽  
Fibroblast Growth ◽  
Distal Chromosome

scholarly journals The Methyl-CpG-binding Protein MeCP2 Links DNA Methylation to Histone Methylation

2002 ◽  
Vol 278 (6) ◽  
pp. 4035-4040 ◽  
Author(s):  
François Fuks ◽  
Paul J. Hurd ◽  
Daniel Wolf ◽  
Xinsheng Nan ◽  
Adrian P. Bird ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Histone Methylation ◽  
Binding Protein ◽  
Protein Mecp2

scholarly journals DNA methylation pathways and their crosstalk with histone methylation

2015 ◽  
Vol 16 (9) ◽  
pp. 519-532 ◽  
Author(s):  
Jiamu Du ◽  
Lianna M. Johnson ◽  
Steven E. Jacobsen ◽  
Dinshaw J. Patel
Keyword(s):  
Dna Methylation ◽  
Histone Methylation
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