ArticlePloS one2015
Transcription driven somatic DNA methylation within the imprinted Gnas cluster.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Bidirectional disruption ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Pseudohypoparathyroidism: complex disease variants with unfortunate names.Journal of molecular endocrinology · 2024Review
- Imprinted Long Non-Coding RNAs in Mammalian Development and Disease.International journal of molecular sciences · 2023Review
- Temporal resolution of gene derepression and proteome changes upon PROTAC-mediated degradation of BCL11A protein in erythroid cells.Cell chemical biology · 2022Article
- Lack of GNAS Remethylation During Oogenesis May Be a Cause of Sporadic Pseudohypoparathyroidism Type Ib.The Journal of clinical endocrinology and metabolism · 2022Article
- Sporadic Pseudohypoparathyroidism Type 1B in Monozygotic Twins: Insights Into the Pathogenesis of Methylation Defects.The Journal of clinical endocrinology and metabolism · 2022Article
- Exploring chromatin structural roles of non-coding RNAs at imprinted domains.Biochemical Society transactions · 2021Review
- Molecular Definition of Pseudohypoparathyroidism Variants.The Journal of clinical endocrinology and metabolism · 2021Review
- A Novel GNAS Duplication Associated With Loss-of-Methylation Restricted to Exon A/B Causes Pseudohypoparathyroidism Type Ib (PHP1B).Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- Methylation changes at theWorld journal of gastrointestinal oncology · 2020Article
- Long noncoding RNA functionality in imprinted domain regulation.PLoS genetics · 2020Review
- Epigenetic transgenerational inheritance of parent-of-origin allelic transmission of outcross pathology and sperm epimutations.Developmental biology · 2020Article
- Meg3-DMR, not the Meg3 gene, regulates imprinting of the Dlk1-Dio3 locus.Developmental biology · 2019Article
- Antisense Activity across theNon-coding RNA · 2015Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Differential marking of genes in female and male gametes by DNA methylation is essential to genomic imprinting. In female gametes transcription traversing differentially methylated regions (DMRs) is a common requirement for de novo methylation at DMRs. At the imprinted Gnas cluster oocyte specific transcription of a protein-coding transcript, Nesp, is needed for methylation of two DMRs intragenic to Nesp, namely the Nespas-Gnasxl DMR and the Exon1A DMR, thereby enabling expression of the Gnas transcript and repression of the Gnasxl transcript. On the paternal allele, Nesp is repressed, the germline DMRs are unmethylated, Gnas is repressed and Gnasxl is expressed. Using mutant mouse models, we show that on the paternal allele, ectopic transcription of Nesp traversing the intragenic Exon1A DMR (which regulates Gnas expression) results in de novo methylation of the Exon1A DMR and de-repression of Gnas just as on the maternal allele. However, unlike the maternal allele, methylation on the mutant paternal allele occurs post-fertilisation, i.e. in somatic cells. This, to our knowledge is the first example of transcript/transcription driven DNA methylation of an intragenic CpG island, in somatic tissues, suggesting that transcription driven de novo methylation is not restricted to the germline in the mouse. Additionally, Gnasxl is repressed on a paternal chromosome on which Nesp is ectopically expressed. Thus, a paternally inherited Gnas cluster showing ectopic expression of Nesp is "maternalised" in terms of Gnasxl and Gnas expression. We show that these mice have a phenotype similar to mutants with two expressed doses of Gnas and none of Gnasxl.
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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.