ArticleNature communications2022
Prematurely terminated intron-retaining mRNAs invade axons in SFPQ null-driven neurodegeneration and are a hallmark of ALS.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 29 citations in OpenAlex.
- Synaptic Proteostasis in Health and Disease.Journal of neurochemistry · 2026Review
- PRMT1-SFPQ regulates intron retention to control matrix gene expression during craniofacial development.eLife · 2026Article
- Spliceosomal component SNRPE drives cell proliferation by regulating CTP synthase 1 mRNA splicing in ovarian cancer.Oncogene · 2026Article
- Targeted blocking of gene splicing can dysregulate intron-embedded primary microRNAs.Communications biology · 2026Article
- Chromatin Meets Condensates: Emerging Interplays Linking Nuclear Paraspeckles to Gene Activation.Epigenetics reports · 2026Article
- Targeting TRIM59 impairs RNA splicing and promotes neuroblastoma differentiation and therapeutic responses.Journal of experimental & clinical cancer research : CR · 2025Article
- Single-nucleus transcriptome atlas of orbitofrontal cortex in ALS with a deep learning-based decoding of alternative polyadenylation mechanisms.Cell genomics · 2025Article
- EIciRNAs in focus: current understanding and future perspectives.RNA biology · 2025Review
- Enhanced hybridization-proximity labeling discovers protein interactomes of single RNA molecules.Nature communications · 2025Article
- Identification and validation of diagnostic alternative splicing events in tumor-educated platelets for non-small cell lung cancer in patients with ground-glass opacity: a multicenter study.Translational lung cancer research · 2025Article
- PRMT5 promotes full-length HTT expression by repressing multiple proximal intronic polyadenylation sites.Nucleic acids research · 2025Article
- Targeting the splicing factor SNRPB inhibits endometrial cancer progression by retaining the POLD1 intron.Experimental & molecular medicine · 2025Article
- Overexpression of SFPQ Improves Cognition and Memory in AD Mice.Neural plasticity · 2025Article
- Deciphering novel mitochondrial signatures: multi-omics analysis uncovers cross-disease markers and oligodendrocyte pathways in Alzheimer's disease and glioblastoma.Frontiers in aging neuroscience · 2025Article
- Serum Splicing Factor Proline- and Glutamine-Rich Is a Diagnostic Marker for Non-Small-Cell Lung Cancer and Other Solid Cancers.International journal of molecular sciences · 2024Article
- Elevated 4R tau contributes to endolysosomal dysfunction and neurodegeneration in VCP-related frontotemporal dementia.Brain : a journal of neurology · 2024Article
- Optimized Primary Culture of Neuronal Populations for Subcellular Omics Applications.Methods in molecular biology (Clifton, N.J.) · 2024Article
- RNA in axons, dendrites, synapses and beyond.Frontiers in molecular neuroscience · 2024Review
- Pathomechanistic Networks of Motor System Injury in Amyotrophic Lateral Sclerosis.Current neuropharmacology · 2024Review
- Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Loss of SFPQ is a hallmark of motor degeneration in ALS and prevents maturation of motor neurons when occurring during embryogenesis. Here, we show that in zebrafish, developing motor neurons lacking SFPQ exhibit axon extension, branching and synaptogenesis defects, prior to degeneration. Subcellular transcriptomics reveals that loss of SFPQ in neurons produces a complex set of aberrant intron-retaining (IR) transcripts coding for neuron-specific proteins that accumulate in neurites. Some of these local IR mRNAs are prematurely terminated within the retained intron (PreT-IR). PreT-IR mRNAs undergo intronic polyadenylation, nuclear export, and localise to neurites in vitro and in vivo. We find these IR and PreT-IR mRNAs enriched in RNAseq datasets of tissue from patients with familial and sporadic ALS. This shared signature, between SFPQ-depleted neurons and ALS, functionally implicates SFPQ with the disease and suggests that neurite-centred perturbation of alternatively spliced isoforms drives the neurodegenerative process.
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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.