ArticlePLoS genetics2020
NCBP2 modulates neurodevelopmental defects of the 3q29 deletion in Drosophila and Xenopus laevis models.
Article in PLoS genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- Review
- Driver or passenger? A new assessment of genes in the schizophrenia-associated 3q29 deletion locus for contribution to neurodevelopmental disorders.Journal of neurodevelopmental disorders · 2026Review
- Suppressive Genetic Interactions Between Haploinsufficient Mitochondrial Genes Encoded in the 22q11.2 Microdeletion Locus Define Brain and Cardiac Phenotypes.bioRxiv : the preprint server for biology · 2026Article
- Comprehensive profiling of RNA modification-related genes identifies RNA mExperimental & molecular medicine · 2025Article
- Downregulation of Pten Improves Huntington's Disease Phenotype by Reducing Htt Aggregates and Cell Death.Molecular neurobiology · 2025Article
- Diversity and consequences of structural variation in the human genome.Nature reviews. Genetics · 2025Review
- NCBP2 predicts the prognosis and the immunotherapy response of cancers: a pan-cancer analysis.PeerJ · 2025Article
- Bioinformatics analysis of the mechanisms of traumatic brain injury-associated dementia based on the competing endogenous RNA.Psychopharmacology · 2024Article
- Flynotyper 2.0: an updated tool for rapid quantitative assessment of Drosophila eye phenotypes.G3 (Bethesda, Md.) · 2024Article
- Flynotyper 2.0: An updated tool for rapid quantitative assessment ofbioRxiv : the preprint server for biology · 2024Article
- A signature of five 7-methylguanosine-related genes is a prognostic marker for lung squamous cell carcinoma.Journal of thoracic disease · 2023Article
- Cross-species analysis identifies mitochondrial dysregulation as a functional consequence of the schizophrenia-associated 3q29 deletion.Science advances · 2023Article
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- Identification of potential pathways and biomarkers linked to progression in ALS.Annals of clinical and translational neurology · 2023Article
- Nuclear import receptors are recruited by FG-nucleoporins to rescue hallmarks of TDP-43 proteinopathy.Molecular neurodegeneration · 2022Article
- Integrated Analysis of Tumor Mutation Burden and Immune Infiltrates in Hepatocellular Carcinoma.Diagnostics (Basel, Switzerland) · 2022Article
- Article
- Ventx Family and Its Functional Similarities with Nanog: Involvement in Embryonic Development and Cancer Progression.International journal of molecular sciences · 2022Review
- Case report: 7p22.3 deletion and 8q24.3 duplication in a patient with epilepsy and psychomotor delay-Does both possibly act to modulate a candidate gene region for the patient's phenotype?Frontiers in genetics · 2022Article
- 16p12.1 Deletion Orthologs are Expressed in Motile Neural Crest Cells and are Important for Regulating Craniofacial Development inFrontiers in genetics · 2022Article
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
The 1.6 Mbp deletion on chromosome 3q29 is associated with a range of neurodevelopmental disorders, including schizophrenia, autism, microcephaly, and intellectual disability. Despite its importance towards neurodevelopment, the role of individual genes, genetic interactions, and disrupted biological mechanisms underlying the deletion have not been thoroughly characterized. Here, we used quantitative methods to assay Drosophila melanogaster and Xenopus laevis models with tissue-specific individual and pairwise knockdown of 14 homologs of genes within the 3q29 region. We identified developmental, cellular, and neuronal phenotypes for multiple homologs of 3q29 genes, potentially due to altered apoptosis and cell cycle mechanisms during development. Using the fly eye, we screened for 314 pairwise knockdowns of homologs of 3q29 genes and identified 44 interactions between pairs of homologs and 34 interactions with other neurodevelopmental genes. Interestingly, NCBP2 homologs in Drosophila (Cbp20) and X. laevis (ncbp2) enhanced the phenotypes of homologs of the other 3q29 genes, leading to significant increases in apoptosis that disrupted cellular organization and brain morphology. These cellular and neuronal defects were rescued with overexpression of the apoptosis inhibitors Diap1 and xiap in both models, suggesting that apoptosis is one of several potential biological mechanisms disrupted by the deletion. NCBP2 was also highly connected to other 3q29 genes in a human brain-specific interaction network, providing support for the relevance of our results towards the human deletion. Overall, our study suggests that NCBP2-mediated genetic interactions within the 3q29 region disrupt apoptosis and cell cycle mechanisms during development.
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