ArticleGenetics2010
A genomic imprinting defect in mice traced to a single gene.
Article in Genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Ventral body wall closure: Mechanistic insights from mouse models and translation to human pathology.Developmental dynamics : an official publication of the American Association of Anatomists · 2025Review
- Epigenetic Mechanisms of ART-Related Imprinting Disorders: Lessons From iPSC and Mouse Models.Genes · 2021Review
- Prenatal correction of IGF2 to rescue the growth phenotypes in mouse models of Beckwith-Wiedemann and Silver-Russell syndromes.Cell reports · 2021Article
- Identification and Tissue-Specific Characterization of Novel SHOX-Regulated Genes in Zebrafish Highlights SOX Family Members Among Other Genes.Frontiers in genetics · 2021Article
- Modeling human epigenetic disorders in mice: Beckwith-Wiedemann syndrome and Silver-Russell syndrome.Disease models & mechanisms · 2020Review
- Increased dosage of the imprinted Ascl2 gene restrains two key endocrine lineages of the mouse Placenta.Developmental biology · 2016Article
- Fetal overgrowth in the Cdkn1c mouse model of Beckwith-Wiedemann syndrome.Disease models & mechanisms · 2011Article
- Chromosome-wide analysis of parental allele-specific chromatin and DNA methylation.Molecular and cellular biology · 2011Article
- Partial loss of Ascl2 function affects all three layers of the mature placenta and causes intrauterine growth restriction.Developmental biology · 2011Article
- MIRA-SNuPE, a quantitative, multiplex method for measuring allele-specific DNA methylation.Epigenetics · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mammalian androgenones have two paternally or sperm-derived genomes. In mice (Mus musculus) they die at peri-implantation due to the misexpression of imprinted genes-the genes that are expressed monoallelically according to the parent of origin. The misexpressions involved are poorly defined. To gain further insight, we examined the causes of midgestation death of embryos with paternal duplication (PatDp) of distal chromosome 7 (dist7), a region replete with imprinted genes. PatDp(dist7) embryos have a similar phenotype to mice with a knockout of a maternally expressed imprinted gene, Ascl2 [achaete-scute complex homolog-like 2 (Drosophila)], and their death at midgestation could result from two inactive paternal copies of this gene. However, other dist7 misexpressions could duplicate this phenotype, and the potential epistatic load is undefined. We show that an Ascl2 transgene is able to promote the development of PatDp(dist7) embryos to term, providing strong evidence that Ascl2 is the only imprinted gene in the genome for which PatDp results in early embryonic death. While some of the defects in perinatal transgenic PatDp(dist7) fetuses were consistent with known misexpressions of dist7 imprinted genes, the overall phenotype indicates a role for additional undefined misexpressions of imprinted genes. This study provides implications for the human imprinting-related fetal overgrowth disorder, Beckwith-Wiedemann syndrome.
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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.