ArticleGenes & development2009
Transcription is required for establishment of germline methylation marks at imprinted genes.
Article in Genes & development, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 179 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
179 citing papers in PubMed, 338 citations in OpenAlex.
- Disruption of KCNQ1 prevents methylation of the ICR2 and supports the hypothesis that its transcription is necessary for imprint establishment.European journal of human genetics : EJHG · 2019Trial
- TET1 noncatalytic activity shapes the chromatin landscape associated with de novo methylation establishment in the male germline.Genes & development · 2026Article
- Establishment of DNA methylation during primate germ cell development.Nature communications · 2026Article
- Multi-omics biomarkers in female fertility: from oocyte quality to endometrial receptivity and clinical translation.Biomarker research · 2026Review
- The superpowers of imprinting control regions.Genome research · 2026Review
- Article
- Preventing CpG hypermethylation in oocytes safeguards mouse development.Developmental cell · 2025Article
- Imprinting and skeletal disorders: lessons from pseudohypoparathyroidism and related disorders.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025Review
- Divergent roles of DNA methylation, TRIM28, and p53 surveillance in human embryonic and trophoblast stem cells.bioRxiv : the preprint server for biology · 2025Article
- An Nlrp5-null mutation leads to attenuated de novo methylation in oocytes, accompanied by a significant reduction in DNMT3L.Molecular human reproduction · 2025Article
- Review
- Maternal loss of mouse Nlrp2 alters the transcriptome and DNA methylome in GV oocytes and impairs zygotic genome activation in embryos.Clinical epigenetics · 2025Article
- Article
- Bidirectional disruption ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- A biallelically active embryonic enhancer dictates GNAS imprinting through allele-specific conformations.Nature communications · 2025Article
- Recurrent small variants in NESP55/NESPAS associated with broad GNAS methylation defects and pseudohypoparathyroidism type 1B.JCI insight · 2024Article
- PRKACB is a novel imprinted gene in marsupials.Epigenetics & chromatin · 2024Article
- Maternal loss-of-function of Nlrp2 results in failure of epigenetic reprogramming in mouse oocytes.Research square · 2024Article
- GNAS AS2 methylation status enables mechanism-based categorization of pseudohypoparathyroidism type 1B.JCI insight · 2024Article
- Pseudohypoparathyroidism: complex disease variants with unfortunate names.Journal of molecular endocrinology · 2024Review
119 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Genomic imprinting requires the differential marking by DNA methylation of genes in male and female gametes. In the female germline, acquisition of methylation imprint marks depends upon the de novo methyltransferase Dnmt3a and its cofactor Dnmt3L, but the reasons why specific sequences are targets for Dnmt3a and Dnmt3L are still poorly understood. Here, we investigate the role of transcription in establishing maternal germline methylation marks. We show that at the Gnas locus, truncating transcripts from the furthest upstream Nesp promoter disrupts oocyte-derived methylation of the differentially methylated regions (DMRs). Transcription through DMRs in oocytes is not restricted to this locus but occurs across the prospective DMRs at many other maternally marked imprinted domains, suggesting a common requirement for transcription events. The transcripts implicated here in gametic methylation are protein-coding, in contrast to the noncoding antisense transcripts involved in the monoallelic silencing of imprinted genes in somatic tissues, although they often initiate from alternative promoters in oocytes. We propose that transcription is a third essential component of the de novo methylation system, which includes optimal CpG spacing and histone modifications, and may be required to create or maintain open chromatin domains to allow the methylation complex access to its preferred targets.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.