ArticlePLoS genetics2006
Recent assembly of an imprinted domain from non-imprinted components.
Article in PLoS genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 84 citations in OpenAlex.
- Insulin secretion deficits in a Prader-Willi syndrome β-cell model are associated with a concerted downregulation of multiple endoplasmic reticulum chaperones.PLoS genetics · 2023Article
- MRKNs: Gene, Functions, and Role in Disease and Infection.Frontiers in oncology · 2022Review
- The Evolutionary Advantage in Mammals of the Complementary Monoallelic Expression Mechanism of Genomic Imprinting and Its Emergence From a Defense Against the Insertion Into the Host Genome.Frontiers in genetics · 2022Review
- Necdin: A purposive integrator of molecular interaction networks for mammalian neuron vitality.Genes to cells : devoted to molecular & cellular mechanisms · 2021Review
- Epigenetics in Prader-Willi Syndrome.Frontiers in genetics · 2021Review
- Evolutionary Conservation of MKRN3 and Other Makorins and Their Roles in Puberty Initiation and Endocrine Functions.Seminars in reproductive medicine · 2019Review
- Snord116-dependent diurnal rhythm of DNA methylation in mouse cortex.Nature communications · 2018Article
- UBE3A: An E3 Ubiquitin Ligase With Genome-Wide Impact in Neurodevelopmental Disease.Frontiers in molecular neuroscience · 2018Review
- Genomic imprinting does not reduce the dosage of UBE3A in neurons.Epigenetics & chromatin · 2017Article
- Early Origin and Evolution of the Angelman Syndrome Ubiquitin Ligase GeneFrontiers in cellular neuroscience · 2017Review
- Genome-wide methylation analysis of retrocopy-associated CpG islands and their genomic environment.Epigenetics · 2016Article
- A new pathway in the control of the initiation of puberty: the MKRN3 gene.Journal of molecular endocrinology · 2015Review
- Genetic differentiation of hypothalamus parentally biased transcripts in populations of the house mouse implicate the Prader-Willi syndrome imprinted region as a possible source of behavioral divergence.Molecular biology and evolution · 2014Article
- Post-natal imprinting: evidence from marsupials.Heredity · 2014Review
- The imprinted NPAP1 gene in the Prader-Willi syndrome region belongs to a POM121-related family of retrogenes.Genome biology and evolution · 2014Article
- Genome-wide histone state profiling of fibroblasts from the opossum, Monodelphis domestica, identifies the first marsupial-specific imprinted gene.BMC genomics · 2014Article
- Article
- Postnatal epigenetic reprogramming in the germline of a marsupial, the tammar wallaby.Epigenetics & chromatin · 2013Article
- The origin and evolution of genomic imprinting and viviparity in mammals.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2013Review
- Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genomic imprinting, representing parent-specific expression of alleles at a locus, raises many questions about how--and especially why--epigenetic silencing of mammalian genes evolved. We present the first in-depth study of how a human imprinted domain evolved, analyzing a domain containing several imprinted genes that are involved in human disease. Using comparisons of orthologous genes in humans, marsupials, and the platypus, we discovered that the Prader-Willi/Angelman syndrome region on human Chromosome 15q was assembled only recently (105-180 million years ago). This imprinted domain arose after a region bearing UBE3A (Angelman syndrome) fused with an unlinked region bearing SNRPN (Prader-Willi syndrome), which had duplicated from the non-imprinted SNRPB/B'. This region independently acquired several retroposed gene copies and arrays of small nucleolar RNAs from different parts of the genome. In their original configurations, SNRPN and UBE3A are expressed from both alleles, implying that acquisition of imprinting occurred after their rearrangement and required the evolution of a control locus. Thus, the evolution of imprinting in viviparous mammals is ongoing.
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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.