ArticleScientific reports2016
Maternal transcription of non-protein coding RNAs from the PWS-critical region rescues growth retardation in mice.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- 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
- Endocrine features of Prader-Willi syndrome: a narrative review focusing on genotype-phenotype correlation.Frontiers in endocrinology · 2024Review
- The emerging role of snoRNAs in human disease.Genes & diseases · 2023Review
- Reference Genes across Nine Brain Areas of Wild Type and Prader-Willi Syndrome Mice: Assessing Differences inInternational journal of molecular sciences · 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
- A Comprehensive Review of Genetically Engineered Mouse Models for Prader-Willi Syndrome Research.International journal of molecular sciences · 2021Review
- Epigenetics in Prader-Willi Syndrome.Frontiers in genetics · 2021Review
- The Role of Long Non-coding RNAs in Human Imprinting Disorders: Prospective Therapeutic Targets.Frontiers in cell and developmental biology · 2021Review
- Functional diversity of small nucleolar RNAs.Nucleic acids research · 2020Article
- Pervasive head-to-tail insertions of DNA templates mask desired CRISPR-Cas9-mediated genome editing events.Science advances · 2020Article
- Ectopic expression of Snord115 in choroid plexus interferes with editing but not splicing of 5-Ht2c receptor pre-mRNA in mice.Scientific reports · 2019Article
- Genotype-Phenotype Relationships and Endocrine Findings in Prader-Willi Syndrome.Frontiers in endocrinology · 2019Review
- Prader-Willi locus Snord116 RNA processing requires an active endogenous allele and neuron-specific splicing by Rbfox3/NeuN.Human molecular genetics · 2018Article
- Neuronal differentiation induces SNORD115 expression and is accompanied by post-transcriptional changes of serotonin receptor 2c mRNA.Scientific reports · 2018Article
- Prader-Willi syndrome and atypical submicroscopic 15q11-q13 deletions with or without imprinting defects.European journal of medical genetics · 2016Article
- Article
- BC1 RNA motifs required for dendritic transport in vivo.Scientific reports · 2016Article
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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) is a neurogenetic disorder caused by loss of paternally expressed genes on chromosome 15q11-q13. The PWS-critical region (PWScr) contains an array of non-protein coding IPW-A exons hosting intronic SNORD116 snoRNA genes. Deletion of PWScr is associated with PWS in humans and growth retardation in mice exhibiting ~15% postnatal lethality in C57BL/6 background. Here we analysed a knock-in mouse containing a 5'HPRT-LoxP-Neo(R) cassette (5'LoxP) inserted upstream of the PWScr. When the insertion was inherited maternally in a paternal PWScr-deletion mouse model (PWScr(p-/m5'LoxP)), we observed compensation of growth retardation and postnatal lethality. Genomic methylation pattern and expression of protein-coding genes remained unaltered at the PWS-locus of PWScr(p-/m5'LoxP) mice. Interestingly, ubiquitous Snord116 and IPW-A exon transcription from the originally silent maternal chromosome was detected. In situ hybridization indicated that PWScr(p-/m5'LoxP) mice expressed Snord116 in brain areas similar to wild type animals. Our results suggest that the lack of PWScr RNA expression in certain brain areas could be a primary cause of the growth retardation phenotype in mice. We propose that activation of disease-associated genes on imprinted regions could lead to general therapeutic strategies in associated diseases.
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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.