ArticleRNA (New York, N.Y.)2017
Mouse models of Casc3 reveal developmental functions distinct from other components of the exon junction complex.
Article in RNA (New York, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Beyond quality control: biological roles of nonsense-mediated RNA decay.The EMBO journal · 2026Review
- MLN51 (Metastatic Lymph Node Gene 51)/CASC3 (Cancer Susceptibility Candidate Gene 3), A Putative Tumour Suppressor in Breast Cancer, the Clinical and Therapeutic Connections.Breast cancer (Dove Medical Press) · 2026Article
- Nonsense-mediated mRNA decay and associated splicing patterns in neurodevelopmental disorders.Frontiers in molecular biosciences · 2026Review
- Gene regulation through exon junction complex modularity.Nature structural & molecular biology · 2025Review
- Nonsense-mediated mRNA decay, a simplified view of a complex mechanism.BMB reports · 2023Review
- An exon junction complex-independent function of Barentsz in neuromuscular synapse growth.EMBO reports · 2022Article
- Exon junction complex dependent mRNA localization is linked to centrosome organization during ciliogenesis.Nature communications · 2021Article
- CASC3 promotes transcriptome-wide activation of nonsense-mediated decay by the exon junction complex.Nucleic acids research · 2020Article
- Article
- The exon junction complex is required for stem and progenitor cell maintenance in planarians.Developmental biology · 2020Article
- Disease modeling of core pre-mRNA splicing factor haploinsufficiency.Human molecular genetics · 2019Article
- The Exon Junction Complex Undergoes a Compositional Switch that Alters mRNP Structure and Nonsense-Mediated mRNA Decay Activity.Cell reports · 2018Article
- RNA on the brain: emerging layers of post-transcriptional regulation in cerebral cortex development.Wiley interdisciplinary reviews. Developmental biology · 2018Review
- Arc 3' UTR Splicing Leads to Dual and Antagonistic Effects in Fine-Tuning Arc Expression Upon BDNF Signaling.Frontiers in molecular neuroscience · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The exon junction complex (EJC) is a multiprotein complex integral to mRNA metabolism. Biochemistry and genetic studies have concluded that the EJC is composed of four core proteins, MAGOH, EIF4A3, RBM8A, and CASC3. Yet recent studies in Drosophila indicate divergent physiological functions for Barentsz, the mammalian Casc3 ortholog, raising the question as to whether CASC3 is a constitutive component of the EJC. This issue remains poorly understood, particularly in an in vivo mammalian context. We previously found that haploinsufficiency for Magoh, Eif4a3, or Rbm8a disrupts neuronal viability and neural progenitor proliferation, resulting in severe microcephaly. Here, we use two new Casc3 mouse alleles to demonstrate developmental phenotypes that sharply contrast those of other core EJC components. Homozygosity for either null or hypomorphic Casc3 alleles led to embryonic and perinatal lethality, respectively. Compound embryos lacking Casc3 expression were smaller with proportionately reduced brain size. Mutant brains contained fewer neurons and progenitors, but no apoptosis, all phenotypes explained by developmental delay. This finding, which contrasts with severe neural phenotypes evident in other EJC mutants, indicates Casc3 is largely dispensable for brain development. In the developing brain, CASC3 protein expression is substoichiometric relative to MAGOH, EIF4A3, and RBM8A. Taken together, this argues that CASC3 is not an essential EJC component in brain development and suggests it could function in a tissue-specific manner.
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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.