ArticleEpigenetics & chromatin2018
Growing oocyte-specific transcription-dependent de novo DNA methylation at the imprinted Zrsr1-DMR.
Article in Epigenetics & chromatin, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 2 citations in OpenAlex.
- Conservation and divergence of canonical and non-canonical imprinting in murids.Genome biology · 2023Pooled it
- Disrupted minor intron splicing activates reductive carboxylation-mediated lipogenesis to drive metabolic dysfunction-associated steatotic liver disease progression.The Journal of clinical investigation · 2025Article
- Identification of responsible sequences which mutations cause maternal H19-ICR hypermethylation with Beckwith-Wiedemann syndrome-like overgrowth.Communications biology · 2024Article
- Review
- Establishment of paternal methylation imprint at theScience advances · 2023Article
- Tissue-specific Grb10/Ddc insulator drives allelic architecture for cardiac development.Molecular cell · 2022Article
- DNA methylation dynamics and dysregulation delineated by high-throughput profiling in the mouse.Cell genomics · 2022Article
- Article
- A human somatic cell culture system for modelling gene silencing by transcriptional interference.Heliyon · 2020Article
- Evolution of imprinting via lineage-specific insertion of retroviral promoters.Nature communications · 2019Article
- A mouse model of Angelman syndrome imprinting defects.Human molecular genetics · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundZrsr1 is a paternally expressed imprinted gene located in the first intron of Commd1, and the Zrsr1 promoter resides in a differentially methylated region (DMR) that is maternally methylated in the oocyte. However, a mechanism for the establishment of the methylation has remained obscure. Commd1 is transcribed in the opposite direction to Zrsr1 with predominant maternal expression, especially in the adult brain.
resultsWe found Commed1 transcribed through the DMR in the growing oocyte. Zrsr1-DMR methylation was abolished by the prevention of Commd1 transcription. Furthermore, methylation did not occur at the artificially unmethylated maternal Zrsr1-DMR during embryonic development when transcription through the DMR was restored in the zygote. Loss of methylation at the maternal Zrsr1-DMR resulted in biallelic Zrsr1 expression and reduced the extent of the predominant maternal expression of Commd1.
conclusionsThese results indicate that the establishment of methylation at Zrsr1-DMR occurs in a transcription-dependent and oocyte-specific manner and caused Zrsr1 imprinting by repressing maternal expression. The predominant maternal expression of Commd1 is likely caused by transcriptional interference by paternal Zrsr1 expression.
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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.