ArticlePLoS genetics2007
Deletion of the MBII-85 snoRNA gene cluster in mice results in postnatal growth retardation.
Article in PLoS genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.
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Who cites it
100 citing papers in PubMed, 1 synthesis or guideline pooled it, 174 citations in OpenAlex.
- Recommendations for the investigation of animal models of Prader-Willi syndrome.Mammalian genome : official journal of the International Mammalian Genome Society · 2013Guideline
- Altered neural electrophysiological properties in the anterior cingulate cortex in a mouse model of Prader-Willi syndrome.The Journal of physiology · 2026Article
- Placental defects revealed by modelling Prader-Willi syndrome in mice.Disease models & mechanisms · 2026Article
- Discovering, Integrating, and Reinterpreting the Molecular Logic of Life: From Classical Theories of Heredity to an Extended Functional Perspective on the Central Dogma.Life (Basel, Switzerland) · 2026Review
- Investigation of a mouse model of Prader-Willi Syndrome with combined disruption of Necdin and Magel2.JCI insight · 2025Article
- Footprints in the Sno: investigating the cellular and molecular mechanisms of SNORD116.Open biology · 2025Review
- Common and Uncommon Mouse Models of Growth Hormone Deficiency.Endocrine reviews · 2024Review
- Newly developed oral bioavailable EHMT2 inhibitor as a potential epigenetic therapy for Prader-Willi syndrome.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Truncated variants of MAGEL2 are involved in the etiologies of the Schaaf-Yang and Prader-Willi syndromes.American journal of human genetics · 2024Article
- Endocrine features of Prader-Willi syndrome: a narrative review focusing on genotype-phenotype correlation.Frontiers in endocrinology · 2024Review
- Coordinated evolution of the SNORD115 and SNORD116 tandem repeats at the imprinted Prader-Willi/Angelman locus.NAR molecular medicine · 2024Article
- Food socialization of children with Prader-Willi syndrome: an interdisciplinary problematization.Frontiers in nutrition · 2023Article
- Analysis ofGenes · 2022Review
- Reference Genes across Nine Brain Areas of Wild Type and Prader-Willi Syndrome Mice: Assessing Differences inInternational journal of molecular sciences · 2022Article
- Probing small ribosomal subunit RNA helix 45 acetylation across eukaryotic evolution.Nucleic acids research · 2022Article
- The contribution of imprinted genes to neurodevelopmental and neuropsychiatric disorders.Translational psychiatry · 2022Review
- Phylogenetic and Molecular Analyses Identify SNORD116 Targets Involved in the Prader-Willi Syndrome.Molecular biology and evolution · 2022Article
- SNORD116 and growth hormone therapy impact IGFBP7 in Prader-Willi syndrome.Genetics in medicine : official journal of the American College of Medical Genetics · 2021Article
- Review
- Comparison of mouse models reveals a molecular distinction between psychotic illness in PWS and schizophrenia.Translational psychiatry · 2021Article
40 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prader-Willi syndrome (PWS [MIM 176270]) is a neurogenetic disorder characterized by decreased fetal activity, muscular hypotonia, failure to thrive, short stature, obesity, mental retardation, and hypogonadotropic hypogonadism. It is caused by the loss of function of one or more imprinted, paternally expressed genes on the proximal long arm of chromosome 15. Several potential PWS mouse models involving the orthologous region on chromosome 7C exist. Based on the analysis of deletions in the mouse and gene expression in PWS patients with chromosomal translocations, a critical region (PWScr) for neonatal lethality, failure to thrive, and growth retardation was narrowed to the locus containing a cluster of neuronally expressed MBII-85 small nucleolar RNA (snoRNA) genes. Here, we report the deletion of PWScr. Mice carrying the maternally inherited allele (PWScr(m-/p+)) are indistinguishable from wild-type littermates. All those with the paternally inherited allele (PWScr(m+/p-)) consistently display postnatal growth retardation, with about 15% postnatal lethality in C57BL/6, but not FVB/N crosses. This is the first example in a multicellular organism of genetic deletion of a C/D box snoRNA gene resulting in a pronounced phenotype.
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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.