Relevant bibliographies by topics / Parent-of-origin-specific Methylation

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Academic literature on the topic 'Parent-of-origin-specific Methylation'

Author: Grafiati
Published: 4 June 2021
Last updated: 3 February 2022

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Journal articles on the topic "Parent-of-origin-specific Methylation"

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Wu, Xin, David A. Galbraith, Paramita Chatterjee, Hyeonsoo Jeong, Christina M. Grozinger, and Soojin V. Yi. "Lineage and Parent-of-Origin Effects in DNA Methylation of Honey Bees (Apis mellifera) Revealed by Reciprocal Crosses and Whole-Genome Bisulfite Sequencing." Genome Biology and Evolution 12, no. 8 (2020): 1482–92. http://dx.doi.org/10.1093/gbe/evaa133.

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Abstract Parent-of-origin methylation arises when the methylation patterns of a particular allele are dependent on the parent it was inherited from. Previous work in honey bees has shown evidence of parent-of-origin-specific expression, yet the mechanisms regulating such pattern remain unknown in honey bees. In mammals and plants, DNA methylation is known to regulate parent-of-origin effects such as genomic imprinting. Here, we utilize genotyping of reciprocal European and Africanized honey bee crosses to study genome-wide allele-specific methylation patterns in sterile and reproductive individuals. Our data confirm the presence of allele-specific methylation in honey bees in lineage-specific contexts but also importantly, though to a lesser degree, parent-of-origin contexts. We show that the majority of allele-specific methylation occurs due to lineage rather than parent-of-origin factors, regardless of the reproductive state. Interestingly, genes affected by allele-specific DNA methylation often exhibit both lineage and parent-of-origin effects, indicating that they are particularly labile in terms of DNA methylation patterns. Additionally, we re-analyzed our previous study on parent-of-origin-specific expression in honey bees and found little association with parent-of-origin-specific methylation. These results indicate strong genetic background effects on allelic DNA methylation and suggest that although parent-of-origin effects are manifested in both DNA methylation and gene expression, they are not directly associated with each other.
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Lefebvre, L., S. Viville, S. C. Barton, F. Ishino, and M. A. Surani. "Genomic Structure and Parent-of-Origin-Specific Methylation of Peg1." Human Molecular Genetics 6, no. 11 (1997): 1907–15. http://dx.doi.org/10.1093/hmg/6.11.1907.

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Golden, Lisa C., Yuichiro Itoh, Noriko Itoh, et al. "Parent-of-origin differences in DNA methylation of X chromosome genes in T lymphocytes." Proceedings of the National Academy of Sciences 116, no. 52 (2019): 26779–87. http://dx.doi.org/10.1073/pnas.1910072116.

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Many autoimmune diseases are more frequent in females than in males in humans and their mouse models, and sex differences in immune responses have been shown. Despite extensive studies of sex hormones, mechanisms underlying these sex differences remain unclear. Here, we focused on sex chromosomes using the “four core genotypes” model in C57BL/6 mice and discovered that the transcriptomes of both autoantigen and anti-CD3/CD28 stimulated CD4+T lymphocytes showed higher expression of a cluster of 5 X genes when derived from XY as compared to XX mice. We next determined if higher expression of an X gene in XY compared to XX could be due to parent-of-origin differences in DNA methylation of the X chromosome. We found a global increase in DNA methylation on the X chromosome of paternal as compared to maternal origin. Since DNA methylation usually suppresses gene expression, this result was consistent with higher expression of X genes in XY cells because XY cells always express from the maternal X chromosome. In addition, gene expression analysis of F1 hybrid mice from CAST × FVB reciprocal crosses showed preferential gene expression from the maternal X compared to paternal X chromosome, revealing that these parent-of-origin effects are not strain-specific. SJL mice also showed a parent-of-origin effect on DNA methylation and X gene expression; however, which X genes were affected differed from those in C57BL/6. Together, this demonstrates how parent-of-origin differences in DNA methylation of the X chromosome can lead to sex differences in gene expression during immune responses.
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Sandovici, Ionel, Sacha Kassovska-Bratinova, J. Concepción Loredo-Osti, et al. "Interindividual variability and parent of origin DNA methylation differences at specific human Alu elements." Human Molecular Genetics 14, no. 15 (2005): 2135–43. http://dx.doi.org/10.1093/hmg/ddi218.

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Gebert, Claudia, David Kunkel, Alexander Grinberg, and Karl Pfeifer. "H19 Imprinting Control Region Methylation Requires an Imprinted Environment Only in the Male Germ Line." Molecular and Cellular Biology 30, no. 5 (2009): 1108–15. http://dx.doi.org/10.1128/mcb.00575-09.

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ABSTRACT The 2.4-kb H19 imprinting control region (H19ICR) is required to establish parent-of-origin-specific epigenetic marks and expression patterns at the Igf2/H19 locus. H19ICR activity is regulated by DNA methylation. The ICR is methylated in sperm but not in oocytes, and this paternal chromosome-specific methylation is maintained throughout development. We recently showed that the H19ICR can work as an ICR even when inserted into the normally nonimprinted alpha fetoprotein locus. Paternal but not maternal copies of the ICR become methylated in somatic tissue. However, the ectopic ICR remains unmethylated in sperm. To extend these findings and investigate the mechanisms that lead to methylation of the H19ICR in the male germ line, we characterized novel mouse knock-in lines. Our data confirm that the 2.4-kb element is an autonomously acting ICR whose function is not dependent on germ line methylation. Ectopic ICRs become methylated in the male germ line, but the timing of methylation is influenced by the insertion site and by additional genetic information. Our results support the idea that DNA methylation is not the primary genomic imprint and that the H19ICR insertion is sufficient to transmit parent-of-origin-dependent DNA methylation patterns independent of its methylation status in sperm.
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Zhao, Guisen, Qingen Yang, Daixin Huang, et al. "Study on the application of parent-of-origin specific DNA methylation markers to forensic genetics." Forensic Science International 154, no. 2-3 (2005): 122–27. http://dx.doi.org/10.1016/j.forsciint.2004.09.123.

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Koetsier, P. A., and W. Doerfler. "Influence of Mouse-Strain-Specific Factors on Position-Dependent Transgene DNA Methylation Patterns." Acta geneticae medicae et gemellologiae: twin research 45, no. 1-2 (1996): 243–44. http://dx.doi.org/10.1017/s0001566000001380.

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In previous work from this laboratory, an inverse dependence was established for the adenovirus type 2 E2A late promoter between sequence-specific DNA methylation and promoter activity [1-5; for reviews see ref. 6, 7]. The effect of DNA methylation on promoter activity was also assessed in the transgenic mice, which were obtained from microinjections of unmethylated or in vitro HpaII-premethylated pAd2E2AL-CAT DNA [1] into F2 zygotes from B6D2F, (C57BL/6 × DBA/2) hybrid mice. In CAT assays carried out on organ extracts from the pAd2E2AL-CAT mice, the inverse relationship was confirmed [2].We studied the stability of the pAd2E2AL-CAT DNA methylation patterns in up to eight mouse generations and assessed the influence of the strain-specific genetic background. Three pAd2E2AL-CAT mouse lines were crossed with inbred DBA/2, C57BL/6 or B6D2F, mice. Parent-of-origin effects were controlled by exclusive hemizygous transgene transmission either via females or males. The founder animal of line 7-1 carried two groups of transgenes (A and B) on separate chromosomes. The transgene methylation patterns of the 7-1B transgenes and those of the lines 5-8 and 8-1 were stably transmitted.Southern blot hybridization experiments [8, 9] revealed that the 7-1A transgene methylation pattern was a cellular mosaic. In mixed-genetic-background offspring from 7-1A animals, 10% carried transgenes with HpaII-DNA methylation levels that were reduced from 40 to 10-15%. This finding suggested that in this background the factors that supported high methylation levels were dominant. When inbred DBA/2 mice were the mates, 40% of the siblings carried demethylated transgenes, whereas this ratio amounted to only 10% in C57BL/6 offspring (comparable to B6D2F1 crossings). Transgene methylation patterns were not detectably influenced by the parent-of-origin.
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Martin, C. Cristofre, and Ross McGowan. "Parent-of-origin specific effects on the methylation of a transgene in the zebrafish,Danio rerio." Developmental Genetics 17, no. 3 (1995): 233–39. http://dx.doi.org/10.1002/dvg.1020170308.

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Li, Li-Lan, Irene Yuk-yee Szeto, Bruce M. Cattanach, Fumitoshi Ishino, and M. Azim Surani. "Organization and Parent-of-Origin-Specific Methylation of Imprinted Peg3 Gene on Mouse Proximal Chromosome 7." Genomics 63, no. 3 (2000): 333–40. http://dx.doi.org/10.1006/geno.1999.6103.

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Szabó, Piroska E., Gerd P. Pfeifer, and Jeffrey R. Mann. "Parent-of-Origin-Specific Binding of Nuclear Hormone Receptor Complexes in the H19-Igf2 Imprinting Control Region." Molecular and Cellular Biology 24, no. 11 (2004): 4858–68. http://dx.doi.org/10.1128/mcb.24.11.4858-4868.2004.

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ABSTRACT Parent-of-origin-specific expression of the mouse insulin-like growth factor 2 gene (Igf2) and the closely linked H19 gene located on distal chromosome 7 is regulated by a 2.4-kb imprinting control region (ICR) located upstream of the H19 gene. In somatic cells, the maternally and paternally derived ICRs are hypo- and hypermethylated, respectively, with the former binding the insulator protein CCCTC-binding factor (CTCF) and acting to block access of enhancers to the Igf2 promoter. Here we report on a detailed in vivo footprinting analysis—using ligation-mediated PCR combined with in vivo dimethyl sulfate, DNase I, or UV treatment—of ICR sequences located outside of the CTCF binding domains. In mouse primary embryo fibroblasts carrying only maternal or paternal copies of distal chromosome 7, we have identified five prominent footprints specific to the maternal ICR. Each of the five footprinted areas contains at least two nuclear hormone receptor hexad binding sites arranged with irregular spacing. When combined with fibroblast nuclear extracts, these sequences interact with complexes containing retinoic X receptor alpha and estrogen receptor beta. More significantly, the footprint sequences bind nuclear hormone receptor complexes in male, but not female, germ cell extracts purified from fetuses at a developmental stage corresponding to the time of establishment of differential ICR methylation. These data are consistent with the possibility that nuclear hormone receptor complexes participate in the establishment of differential ICR methylation imprinting in the germ line.
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Dissertations / Theses on the topic "Parent-of-origin-specific Methylation"

1

Shapiro, Jonathan. "A Novel Approach to Identify Candidate Imprinted Genes in Humans." Thesis, 2012. http://hdl.handle.net/1807/32278.

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Many imprinted genes are necessary for normal human development. Approximately 70 imprinted genes have been identified in humans. I developed a novel approach to identify candidate imprinted genes in humans using the premise that imprinted genes are often associated with nearby parent-of-origin-specific DNA differentially methylated regions (DMRs). I identified parent-of-origin-specific DMRs using sodium bisulfite-based DNA (CpG) methylation profiling of uniparental tissues, mature cystic ovarian teratoma (MCT) and androgenetic complete hydatidiform mole (AnCHM), and biparental tissues, blood and placenta. In support of this approach, the CpG methylation profiling led to the identification of parent-of-origin-specific differentially methylated CpG sites (DMCpGs) in known parent-of-origin-specific DMRs. I found new DMRs for known imprinted genes NAP1L5 and ZNF597. Most importantly, I discovered many new DMCpGs, which were associated with nearby genes, i.e., candidate imprinted genes. Allelic expression analyses of one candidate imprinted gene, AXL, suggested polymorphic imprinting of AXL in human blood.
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