ReviewInternational journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience2016
Alternative splicing and nonsense-mediated mRNA decay enforce neural specific gene expression.
Review in International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 69 citations in OpenAlex.
- A novel synonymous TSC2 mutation in a Chinese family leads to tuberous sclerosis type 2 by disrupting Normal pre-mRNA splicing.Journal, genetic engineering & biotechnology · 2026Article
- Predicting nonsense-mediated mRNA decay from splicing events in sepsis using RNA-sequencing data.Life science alliance · 2025Article
- Direct and indirect effects of spliceosome disruption compromise gene regulation by nonsense-mediated mRNA decay.RNA biology · 2025Article
- The implications of alternative splicing regulation for maximum lifespan.Nature communications · 2025Article
- The Implications of Alternative Splicing Regulation for Maximum Lifespan.bioRxiv : the preprint server for biology · 2025Article
- Tri-snRNP activity modulates tauopathy phenotypes.NAR molecular medicine · 2025Article
- Human introns contain conserved tissue-specific cryptic poison exons.NAR genomics and bioinformatics · 2024Article
- Study of the RNA splicing kinetics via in vivo 5-EU labeling.RNA (New York, N.Y.) · 2024Article
- Article
- Article
- Global impact of aberrant splicing on human gene expression levels.bioRxiv : the preprint server for biology · 2023Article
- Cryptic exon detection and transcriptomic changes revealed in single-nuclei RNA sequencing of C9ORF72 patients spanning the ALS-FTD spectrum.Acta neuropathologica · 2023Article
- Mapping genetic variants for nonsense-mediated mRNA decay regulation across human tissues.Genome biology · 2023Article
- Tissue-specific regulation of gene expression via unproductive splicing.Nucleic acids research · 2023Article
- Article
- Diverse Roles of the Exon Junction Complex Factors in the Cell Cycle, Cancer, and Neurodevelopmental Disorders-Potential for Therapeutic Targeting.International journal of molecular sciences · 2022Review
- Survey of the binding preferences of RNA-binding proteins to RNA editing events.Genome biology · 2022Article
- Multilayered regulations of alternative splicing, NMD, and protein stability control temporal induction and tissue-specific expression of TRIM46 during axon formation.Nature communications · 2022Article
- Quantitative Measurement of Alternatively Spliced RNA Isoform Levels.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Brain-trait-associated variants impact cell-type-specific gene regulation during neurogenesis.American journal of human genetics · 2021Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Alternative pre-mRNA splicing is a fundamental regulatory process for most mammalian multi-exon genes to increase proteome diversity. Nonsense-mediated mRNA decay (NMD) is a conserved mRNA surveillance mechanism to mitigate deleterious effects caused by gene mutations or transcriptional errors. Coupling alternative splicing and NMD (AS-NMD), in which alternative splicing switches between translational and NMD isoforms, results in fine-tuning overall gene expression to, in turn, expand the functional activities of these two post-transcriptional regulatory processes. AS-NMD is known for maintaining homeostatic expression of many RNA-binding proteins. We further show that AS-NMD is a conserved mechanism among mammals to induce developmental expression of the synaptic scaffold protein PSD-95. Comparing gene sequences between human Psd-95 and its ancestral orthologues indicates that AS-NMD regulation of mammalian Psd-95 is a product of selective pressure and that it enforces neural-specific expression of PSD-95 proteins in mammals. Invertebrate homolog of Psd-95 is not subjected to AS-NMD regulation and its protein product does not exhibit neural-specific expression. Given the prevalence of alternative splicing regulation in the mammalian nervous system, neural-specific expression of many other genes could be controlled by AS-NMD in a similar manner. We discuss the implication of these discoveries, as well as the challenges in generalizing the regulation and functional activity of AS-NMD.
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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.