ArticleProceedings of the National Academy of Sciences of the United States of America2015
Regulation of DLK1 by the maternally expressed miR-379/miR-544 cluster may underlie callipyge polar overdominance inheritance.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 42 citations in OpenAlex.
- Combinatorial targeting of the miR-379/miR-410 cluster normalizes glucose and lipid homeostasis in male models of diabetes and obesity.Nature communications · 2026Article
- The long non-coding RNA Meg3 mediates imprinted gene expression during stem cell differentiation.Nucleic acids research · 2024Article
- Dlk1-Dio3 cluster miRNAs regulate mitochondrial functions in the dystrophic muscle in Duchenne muscular dystrophy.Life science alliance · 2023Article
- Epigenetic changes induced by in utero dietary challenge result in phenotypic variability in successive generations of mice.Nature communications · 2022Article
- miRNAs as markers for the development of individualized training regimens: A pilot study.Physiological reports · 2022Article
- A revised model for mitochondrial dysfunction in Duchenne muscular dystrophy.European journal of translational myology · 2021Article
- Exploring chromatin structural roles of non-coding RNAs at imprinted domains.Biochemical Society transactions · 2021Review
- Molecular Mechanisms of Skeletal Muscle Hypertrophy.Journal of neuromuscular diseases · 2021Review
- Lack ofFrontiers in cell and developmental biology · 2021Article
- Multi-Omics Identifies Circulating miRNA and Protein Biomarkers for Facioscapulohumeral Dystrophy.Journal of personalized medicine · 2020Article
- Deficiency and overexpression ofDevelopment (Cambridge, England) · 2020Article
- Long noncoding RNA functionality in imprinted domain regulation.PLoS genetics · 2020Review
- Expression Levels of Long Non-Coding RNAs Change in Models of Altered Muscle Activity and Muscle Mass.International journal of molecular sciences · 2020Article
- Meg3-DMR, not the Meg3 gene, regulates imprinting of the Dlk1-Dio3 locus.Developmental biology · 2019Article
- Retrotransposon gag-like 1 (RTL1) and the molecular evolution of self-targeting imprinted microRNAs.Biology direct · 2019Article
- Expression and Functional Analyses of Dlk1 in Muscle Stem Cells and Mesenchymal Progenitors during Muscle Regeneration.International journal of molecular sciences · 2019Article
- Clonal derivation of white and brown adipocyte progenitor cell lines from human pluripotent stem cells.Stem cell research & therapy · 2019Article
- A Hearty Dose of Noncoding RNAs: The ImprintedJournal of cardiovascular development and disease · 2018Review
- Identification of genes directly responding to DLK1 signaling in Callipyge sheep.BMC genomics · 2018Article
- Small-RNA sequencing identifies dynamic microRNA deregulation during skeletal muscle lineage progression.Scientific reports · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inheritance of the callipyge phenotype in sheep is an example of polar overdominance inheritance, an unusual mode of inheritance. To investigate the underlying molecular mechanism, we profiled the expression of the genes located in the Delta-like 1 homolog (Dlk1)-type III iodothyronine deiodinase (Dio3) imprinting region in mice. We found that the transcripts of the microRNA (miR) 379/miR-544 cluster were highly expressed in neonatal muscle and paralleled the expression of the Dlk1. We then determined the in vivo role of the miR-379/miR-544 cluster by establishing a mouse line in which the cluster was ablated. The maternal heterozygotes of young mutant mice displayed a hypertrophic tibialis anterior muscle, extensor digitorum longus muscle, gastrocnemius muscle, and gluteus maximus muscle and elevated expression of the DLK1 protein. Reduced expression of DLK1 was mediated by miR-329, a member of this cluster. Our results suggest that maternal expression of the imprinted miR-379/miR-544 cluster regulates paternal expression of the Dlk1 gene in mice. We therefore propose a miR-based molecular working model for polar overdominance inheritance.
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.