Chromatin regulators of genomic imprinting

Weaver, Jamie R.; Bartolomei, Marisa S.

doi:10.1016/j.bbagrm.2013.12.002

Cited by 44 publications

(34 citation statements)

References 106 publications

(139 reference statements)

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“…PcG proteins maintain repression, whereas TrxG proteins promote gene activity (1)(2)(3)(4). Misregulation of PcG and TrxG genes leads to abnormalities in development and cancer (5)(6)(7)(8).…”

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confidence: 99%

Transcriptional read-through is not sufficient to induce an epigenetic switch in the silencing activity of Polycomb response elements

Erokhin

Elizar’ev

Parshikov

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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In Drosophila, Polycomb (PcG) and Trithorax (TrxG) group proteins are assembled on Polycomb response elements (PREs) to maintain tissue and stage-specific patterns of gene expression. Critical to coordinating gene expression with the process of differentiation, the activity of PREs can be switched "on" and "off." When on, the PRE imposes a silenced state on the genes in the same domain that is stably inherited through multiple rounds of cell division. When the PRE is switched off, the domain is in a state permissive for gene expression that can be stably inherited. Previous studies have suggested that a burst of transcription through a PRE sequence displaces PcG proteins and provides a universal mechanism for inducing a heritable switch in PRE activity from on to off; however, the evidence favoring this model is indirect. Here, we have directly tested the transcriptional read-through mechanism. Contrary to previous suggestions, we show that transcription through the PRE is not sufficient for inducing an epigenetic switch in PRE activity. In fact, even high levels of continuous transcription through a PRE fails to dislodge the PcG proteins, nor does it remove repressive histone marks. Our results indicate that other mechanisms involving adjacent DNA regulatory elements must be implicated in heritable switch of PRE activity.Polycomb | chromatin silencing | bithorax | intergenic transcription | Trithorax

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mentioning

confidence: 99%

Transcriptional read-through is not sufficient to induce an epigenetic switch in the silencing activity of Polycomb response elements

Erokhin

Elizar’ev

Parshikov

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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“…In addition, the imprinting control region of KCNQ1 gene includes the promoter of the Kcnq1ot1 long non‐coding RNA (ncRNA). The paternal imprinting control region is unmethylated, which allows the ncRNA Kcnq1ot1 to transcript, and then silences the paternal alleles of the adjacent genes (Plasschaert & Bartolomei, ; Weaver & Bartolomei, ).…”

Section: Discussionmentioning

confidence: 99%

Methylation levels ofIGF2andKCNQ1in spermatozoa from infertile men are associated with sperm DNA damage

Pan

et al. 2019

Andrologia

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Abnormal imprinted genes methylation in spermatozoa has been shown to be associated with subfertility. However, the relationship between sperm DNA damage and specific imprinted genes methylation remains unclear. In this study, DNA methylation levels were determined at seven imprinted genes loci (H19, INS‐IGF2, KCNQ1, MEG3, MEST, PEG3 and SNRPN) in 66 semen samples using the MSRE‐qPCR method. The semen samples were divided into two groups according to the threshold value (25%) of DNA fragmentation index (DFI). We found that the mean methylation level at IGF2 (cg17037101) in the group with DFI ≥ 25% was lower than that in the group with DFI < 25% (13.7 ± 3% vs. 31.5 ± 5.3%, p = 0.0053). However, the methylation levels of other CpGs did not differ from the imprinted genes. Correlation analysis of DFI with the methylation levels of imprinted genes demonstrated that the IGF2 (cg17037101) methylation level was negatively correlated with sperm DFI (r = −0.448, p = 0.0038), and the KCNQ1 (cg24932449) methylation level was positively correlated with sperm DFI (r = 0.354, p = 0.0273). Our results suggest that the aberrant methylation of IGF2 and KCNQ1 genes may be associated with sperm DNA damage.

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“…Changes in epigenetic modifications contribute to stable alterations in gene expression. Imprinted genes are associated with multiple layers of epigenetic regulation, including DNA methylation at differentially methylated regions (DMRs) and histone modifications, resulting in monoallelic expression (Weaver & Bartolomei 2014). IGF2 is one of the well-studied maternally imprinted genes expressed in maternal, fetal and placental tissues during early pregnancy contributing to fetal growth.…”

Section: R234mentioning

confidence: 99%

Progress in the understanding of the etiology and predictability of fetal growth restriction

Tang

Liu

et al. 2017

Reproduction

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Fetal growth restriction (FGR) is defined as the failure of fetus to reach its growth potential for various reasons, leading to multiple perinatal complications and adult diseases of fetal origins. Shallow extravillous trophoblast (EVT) invasion-induced placental insufficiency and placental dysfunction are considered the main reasons for idiopathic FGR. In this review, first we discuss the major characteristics of anti-angiogenic state and the pro-inflammatory bias in FGR. We then elaborate major abnormalities in placental insufficiency at molecular levels, including the interaction between decidual leukocytes and EVT, alteration of miRNA expression and imprinted gene expression pattern in FGR. Finally, we review current animal models used in FGR, an experimental intervention based on animal models and the progress of predictive biomarker studies in FGR. Free Chinese abstract: A Chinese translation of this abstract is freely available at http://www.reproduction-online.org/content/153/6/ R227/suppl/DC1. Reproduction (2017) 153 R227-R240

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Chromatin regulators of genomic imprinting

Cited by 44 publications

References 106 publications

Transcriptional read-through is not sufficient to induce an epigenetic switch in the silencing activity of Polycomb response elements

Transcriptional read-through is not sufficient to induce an epigenetic switch in the silencing activity of Polycomb response elements

Methylation levels ofIGF2andKCNQ1in spermatozoa from infertile men are associated with sperm DNA damage

Progress in the understanding of the etiology and predictability of fetal growth restriction

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