ArticleRNA (New York, N.Y.)2013
Developmental arrest of Drosophila survival motor neuron (Smn) mutants accounts for differences in expression of minor intron-containing genes.
Article in RNA (New York, N.Y.), 2013. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 51 citations in OpenAlex.
- The minor spliceosome component U4atac regulates JAK/STAT signaling to modulate hematopoiesis and immune responses in Drosophila melanogaster.Nature communications · 2026Article
- 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
- Therapy development for spinal muscular atrophy: perspectives for muscular dystrophies and neurodegenerative disorders.Neurological research and practice · 2022Review
- Identification and structural analysis of the Schizosaccharomyces pombe SMN complex.Nucleic acids research · 2021Article
- Defective minor spliceosomes induce SMA-associated phenotypes through sensitive intron-containing neural genes in Drosophila.Nature communications · 2020Article
- 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
- Functional characterization of SMN evolution in mouse models of SMA.Scientific reports · 2019Article
- Comprehensive Modeling of Spinal Muscular Atrophy inFrontiers in molecular neuroscience · 2019Article
- Defective Expression of Mitochondrial, Vacuolar HFrontiers in genetics · 2019Article
- Self-oligomerization regulates stability of survival motor neuron protein isoforms by sequestering an SCFMolecular biology of the cell · 2018Article
- SMN regulation in SMA and in response to stress: new paradigms and therapeutic possibilities.Human genetics · 2017Review
- Developmental regulation of SMN expression: pathophysiological implications and perspectives for therapy development in spinal muscular atrophy.Gene therapy · 2017Review
- Impaired spliceosomal UsnRNP assembly leads to Sm mRNA down-regulation and Sm protein degradation.The Journal of cell biology · 2017Article
- Towards an understanding of regulating Cajal body activity by protein modification.RNA biology · 2017Review
- SMN - A chaperone for nuclear RNP social occasions?RNA biology · 2017Review
- A newRNA (New York, N.Y.) · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Reduced levels of survival motor neuron (SMN) protein lead to a neuromuscular disease called spinal muscular atrophy (SMA). Animal models of SMA recapitulate many aspects of the human disease, including locomotion and viability defects, but have thus far failed to uncover the causative link between a lack of SMN protein and neuromuscular dysfunction. While SMN is known to assemble small nuclear ribonucleoproteins (snRNPs) that catalyze pre-mRNA splicing, it remains unclear whether disruptions in splicing are etiologic for SMA. To investigate this issue, we carried out RNA deep-sequencing (RNA-seq) on age-matched Drosophila Smn-null and wild-type larvae. Comparison of genome-wide mRNA expression profiles with publicly available data sets revealed the timing of a developmental arrest in the Smn mutants. Furthermore, genome-wide differences in splicing between wild-type and Smn animals did not correlate with changes in mRNA levels. Specifically, we found that mRNA levels of genes that contain minor introns vary more over developmental time than they do between wild-type and Smn mutants. An analysis of reads mapping to minor-class intron-exon junctions revealed only small changes in the splicing of minor introns in Smn larvae, within the normal fluctuations that occur throughout development. In contrast, Smn mutants displayed a prominent increase in levels of stress-responsive transcripts, indicating a systemic response to the developmental arrest induced by loss of SMN protein. These findings not only provide important mechanistic insight into the developmental arrest displayed by Smn mutants, but also argue against a minor-intron-dependent etiology for SMA.
Indexed as
Identifiers
What OpenQuestion holds
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.