ArticleNature communications2021
Genetic dissection identifies Necdin as a driver gene in a mouse model of paternal 15q duplications.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Haplotype-resolved methylomes reveal parent-of-origin DNA methylation imbalance in autism spectrum disorder.Science advances · 2026Article
- Dup15q model mice exhibit impaired gastrointestinal motility and a constipation-like phenotype, alleviated by prucalopride.Translational psychiatry · 2026Article
- Review
- Neonatal social communication and single genes predict the variability of post-pubertal social behavior in a mouse model of paternal 15q11-13 duplication.Research square · 2026Article
- Loss of Necdin causes social deficit and aberrant synaptic function through destabilization of SynGAP.Molecular psychiatry · 2026Article
- Deciphering copy number variations and gene implications in an Egyptian cohort with autism spectrum disorders.BMC medical genomics · 2025Article
- Neurometabolic profiles of autism spectrum disorder patients with genetic variants in specific neurotransmission and synaptic genes.Scientific reports · 2025Article
- Investigation of a mouse model of Prader-Willi Syndrome with combined disruption of Necdin and Magel2.JCI insight · 2025Article
- Case Report: Prenatal diagnosis of 10 fetuses with 15q11-q13 duplication and pregnancy outcome in a cohort of Chinese women.Frontiers in neuroscience · 2025Article
- Spatial Cell Atlas of Lateral Septum Reveals Changes Underlying Anxiety and Fear Learning Deficits in Mice with Abnormal Immunity.International journal of biological sciences · 2025Article
- Mechanisms of copy number variants in neuropsychiatric disorders: From genes to therapeutics.Current opinion in neurobiology · 2023Review
- CNTNAP2 intracellular domain (CICD) generated by γ-secretase cleavage improves autism-related behaviors.Signal transduction and targeted therapy · 2023Article
- The role of UBE3A in the autism and epilepsy-related Dup15q syndrome using patient-derived, CRISPR-corrected neurons.Stem cell reports · 2023Article
- Molecular and behavioral consequences of Ube3a gene overdosage in mice.JCI insight · 2022Article
- Small Extracellular Vesicles in Milk Cross the Blood-Brain Barrier in Murine Cerebral Cortex Endothelial Cells and Promote Dendritic Complexity in the Hippocampus and Brain Function in C57BL/6J Mice.Frontiers in nutrition · 2022Article
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maternally inherited duplication of chromosome 15q11-q13 (Dup15q) is a pathogenic copy number variation (CNV) associated with autism spectrum disorder (ASD). Recently, paternally derived duplication has also been shown to contribute to the development of ASD. The molecular mechanism underlying paternal Dup15q remains unclear. Here, we conduct genetic and overexpression-based screening and identify Necdin (Ndn) as a driver gene for paternal Dup15q resulting in the development of ASD-like phenotypes in mice. An excess amount of Ndn results in enhanced spine formation and density as well as hyperexcitability of cortical pyramidal neurons. We generate 15q dupΔNdn mice with a normalized copy number of Ndn by excising its one copy from Dup15q mice using a CRISPR-Cas9 system. 15q dupΔNdn mice do not show ASD-like phenotypes and show dendritic spine dynamics and cortical excitatory-inhibitory balance similar to wild type animals. Our study provides an insight into the role of Ndn in paternal 15q duplication and a mouse model of paternal Dup15q syndrome.
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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.