ArticleRNA (New York, N.Y.)2016
Transcriptomic comparison of Drosophila snRNP biogenesis mutants reveals mutant-specific changes in pre-mRNA processing: implications for spinal muscular atrophy.
Article in RNA (New York, N.Y.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Biphasic SMN condensates safeguard stress-induced cytoplasmic mislocalization of splicing RNPs.Cellular and molecular life sciences : CMLS · 2026Article
- PHAX enhanced LIN28B-mediated PBX3 mRNA stability to promote esophageal cancer development.Cancer science · 2025Article
- Chaperoning the chaperones: Proteomic analysis of the SMN complex reveals conserved and etiologic connections to the proteostasis network.bioRxiv : the preprint server for biology · 2024Article
- Dysregulation of innate immune signaling in animal models of spinal muscular atrophy.BMC biology · 2024Article
- Proteomic analysis of the SMN complex reveals conserved and etiologic connections to the proteostasis network.Frontiers in RNA research · 2024Article
- Dysregulation of innate immune signaling in animal models of Spinal Muscular Atrophy.bioRxiv : the preprint server for biology · 2023Article
- Allele-specific alternative splicing of Drosophila Ribosomal protein S21 suppresses a lethal mutation in the Phosphorylated adaptor for RNA export (Phax) gene.G3 (Bethesda, Md.) · 2022Article
- The nuclear cap-binding complex as choreographer of gene transcription and pre-mRNA processing.Genes & development · 2020Review
- Temperature-sensitive spinal muscular atrophy-causing point mutations lead to SMN instability, locomotor defects and premature lethality inDisease models & mechanisms · 2020Article
- Intimate functional interactions between TGS1 and the Smn complex revealed by an analysis of the Drosophila eye development.PLoS genetics · 2020Article
- Composition of the Survival Motor Neuron (SMN) Complex inG3 (Bethesda, Md.) · 2019Article
- Dissecting Motor Neuron Disease WithFrontiers in neuroscience · 2019Review
- Defective Expression of Mitochondrial, Vacuolar HFrontiers in genetics · 2019Article
- Comprehensive Modeling of Spinal Muscular Atrophy inFrontiers in molecular neuroscience · 2019Article
- Arabidopsis RNA processing factor SERRATE regulates the transcription of intronless genes.eLife · 2018Article
- mRNP assembly, axonal transport, and local translation in neurodegenerative diseases.Brain research · 2018Review
- Self-oligomerization regulates stability of survival motor neuron protein isoforms by sequestering an SCFMolecular biology of the cell · 2018Article
- Ovule identity mediated by pre-mRNA processing in Arabidopsis.PLoS genetics · 2018Article
- SMN - A chaperone for nuclear RNP social occasions?RNA biology · 2017Review
- SMN deficiency in severe models of spinal muscular atrophy causes widespread intron retention and DNA damage.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Survival motor neuron (SMN) functions in the assembly of spliceosomal small nuclear ribonucleoproteins (snRNPs) that catalyze pre-mRNA splicing. Here, we used disruptions in Smn and two additional snRNP biogenesis genes, Phax and Ars2, to classify RNA processing differences as snRNP-dependent or gene-specific in Drosophila Phax and Smn mutants exhibited comparable reductions in snRNAs, and comparison of their transcriptomes uncovered shared sets of RNA processing changes. In contrast, Ars2 mutants displayed only small decreases in snRNA levels, and RNA processing changes in these mutants were generally distinct from those identified in Phax and Smn animals. Instead, RNA processing changes in Ars2 mutants support the known interaction of Ars2 protein with the cap-binding complex, as splicing changes showed a clear bias toward the first intron. Bypassing disruptions in snRNP biogenesis, direct knockdown of spliceosomal proteins caused similar changes in the splicing of snRNP-dependent events. However, these snRNP-dependent events were largely unaltered in three Smn mutants expressing missense mutations that were originally identified in human spinal muscular atrophy (SMA) patients. Hence, findings here clarify the contributions of Phax, Smn, and Ars2 to snRNP biogenesis in Drosophila, and loss-of-function mutants for these proteins reveal differences that help disentangle cause and effect in SMA model flies.
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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.