ArticleHuman molecular genetics2017
Loss of the imprinted, non-coding Snord116 gene cluster in the interval deleted in the Prader Willi syndrome results in murine neuronal and endocrine pancreatic developmental phenotypes.
Article in Human molecular genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Oxytocin in infants with Prader-Willi syndrome to improve dysphagia and disease trajectory.Orphanet journal of rare diseases · 2026Trial
- Article
- Altered neural electrophysiological properties in the anterior cingulate cortex in a mouse model of Prader-Willi syndrome.The Journal of physiology · 2026Article
- Systematic mapping of small nucleolar RNA interactions in human cells.RNA biology · 2025Article
- Neuroendocrinology and the Genetics of Obesity.Endocrinology · 2025Review
- Unlocking the life code: a review of SnoRNA functional diversity and disease relevance.Cell communication and signaling : CCS · 2025Review
- Light and sex modifybioRxiv : the preprint server for biology · 2025Article
- Footprints in the Sno: investigating the cellular and molecular mechanisms of SNORD116.Open biology · 2025Review
- Roles of SNORD115 and SNORD116 ncRNA clusters during neuronal differentiation.Nature communications · 2024Article
- NOCICEPTRA2.0 - A comprehensive ncRNA atlas of human native and iPSC-derived sensory neurons.iScience · 2023Article
- The emerging role of snoRNAs in human disease.Genes & diseases · 2023Review
- Cardiovascular complications of diabetes: role of non-coding RNAs in the crosstalk between immune and cardiovascular systems.Cardiovascular diabetology · 2023Review
- A Comprehensive Review of Genetically Engineered Mouse Models for Prader-Willi Syndrome Research.International journal of molecular sciences · 2021Review
- What can we learn from PWS and SNORD116 genes about the pathophysiology of addictive disorders?Molecular psychiatry · 2021Review
- Emerging Classes of Small Non-Coding RNAs With Potential Implications in Diabetes and Associated Metabolic Disorders.Frontiers in endocrinology · 2021Review
- The Role of Long Non-coding RNAs in Human Imprinting Disorders: Prospective Therapeutic Targets.Frontiers in cell and developmental biology · 2021Review
- Interpreting the impact of noncoding structural variation in neurodevelopmental disorders.Genetics in medicine : official journal of the American College of Medical Genetics · 2021Review
- Transcriptome analysis identifies putative multi-gene signature distinguishing benign and malignant pancreatic head mass.Journal of translational medicine · 2020Article
- Death by lipids: The role of small nucleolar RNAs in metabolic stress.The Journal of biological chemistry · 2020Review
- Functional diversity of small nucleolar RNAs.Nucleic acids research · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Global neurodevelopmental delay is a prominent characteristic of individuals with Prader-Willi syndrome (PWS). The neuromolecular bases for these delays are unknown. We identified neuroanatomical changes in the brains of mice deficient for a gene in the minimal critical deletion region for PWS (Snord116p-/m+). In Snord116p-/m+ mice, reduced primary forebrain neuron cell body size is apparent in embryonic day 15.5 fetuses, and persists until postnatal day 30 in cerebellar Purkinje neurons. Snord116 is a snoRNA gene cluster of unknown function that can localize to the nucleolus. In cerebellar Purkinje neurons from postnatal day 30 Snord116p-/m+ mice the reduction in neuronal cell body size was associated with decreased neuronal nucleolar size. We also identified developmental changes in the endocrine pancreas of Snord116p-/m+ animals that persist into adulthood. Mice lacking Snord116 have smaller pancreatic islets; within the islet the percentage of δ-cells is increased, while the percentage of α-cells is reduced. The α-cell markers, Sst and Hhex, are upregulated in Snord116p-/m+ isolated islets while Ins1, Ins2, Pdx1, Nkx6-1, and Pax6 are downregulated. There is a 3-fold increase in the percentage of polyhormonal cells in the neonatal pancreata of Snord116p-/m+ mice, due primarily to an increase in cells co-positive with somatostatin. Snord116 may play a role in islet cell lineage specification. The Snord116 gene cluster is important for developmental processes in the brain as well as the endocrine pancreas.
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Registered trials
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