ArticlePloS one2010
Gene expression profiling of U12-type spliceosome mutant Drosophila reveals widespread changes in metabolic pathways.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Connecting genotype and phenotype in minor spliceosome diseases.RNA (New York, N.Y.) · 2025Review
- Zrsr2 Is Essential for the Embryonic Development and Splicing of Minor Introns in RNA and Protein Processing Genes in Zebrafish.International journal of molecular sciences · 2022Article
- Prohibitins in neurodegeneration and mitochondrial homeostasis.Frontiers in aging · 2022Review
- RNA Binding Motif Protein 48 Is Required for U12 Splicing and Maize Endosperm Differentiation.The Plant cell · 2019Article
- An Integrated Model of Minor Intron Emergence and Conservation.Frontiers in genetics · 2019Article
- Alternative exon definition events control the choice between nuclear retention and cytoplasmic export of U11/U12-65K mRNA.PLoS genetics · 2017Article
- Aberrant splicing in maizeProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Evolutionarily conserved exon definition interactions with U11 snRNP mediate alternative splicing regulation on U11-48K and U11/U12-65K genes.RNA biology · 2015Article
- Global analysis of the nuclear processing of transcripts with unspliced U12-type introns by the exosome.Nucleic acids research · 2014Article
- Minor class splicing shapes the zebrafish transcriptome during development.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Developmental arrest of Drosophila survival motor neuron (Smn) mutants accounts for differences in expression of minor intron-containing genes.RNA (New York, N.Y.) · 2013Article
- Microcephalic osteodysplastic primordial dwarfism type I with biallelic mutations in the RNU4ATAC gene.Clinical genetics · 2012Article
- A Drosophila model of spinal muscular atrophy uncouples snRNP biogenesis functions of survival motor neuron from locomotion and viability defects.Cell reports · 2012Article
- Gene expression analysis of Drosophilaa Manf mutants reveals perturbations in membrane traffic and major metabolic changes.BMC genomics · 2012Article
- New connections between splicing and human disease.Trends in genetics : TIG · 2012Review
- Mechanisms and pathways of growth failure in primordial dwarfism.Genes & development · 2011Review
- Mutations in U4atac snRNA, a component of the minor spliceosome, in the developmental disorder MOPD I.Science (New York, N.Y.) · 2011Article
- The significant other: splicing by the minor spliceosome.Wiley interdisciplinary reviews. RNAReview
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe U12-type spliceosome is responsible for the removal of a subset of introns from eukaryotic mRNAs. U12-type introns are spliced less efficiently than normal U2-type introns, which suggests a rate-limiting role in gene expression. The Drosophila genome contains about 20 U12-type introns, many of them in essential genes, and the U12-type spliceosome has previously been shown to be essential in the fly. METHODOLOGY/PRINCIPAL
findingsWe have used a Drosophila line with a P-element insertion in U6atac snRNA, an essential component of the U12-type spliceosome, to investigate the impact of U12-type introns on gene expression at the organismal level during fly development. This line exhibits progressive accumulation of unspliced U12-type introns during larval development and the death of larvae at the third instar stage. Surprisingly, microarray and RT-PCR analyses revealed that most genes containing U12-type introns showed only mild perturbations in the splicing of U12-type introns. In contrast, we detected widespread downstream effects on genes that do not contain U12-type introns, with genes related to various metabolic pathways constituting the largest group. CONCLUSIONS/SIGNIFICANCE: U12-type intron-containing genes exhibited variable gene-specific responses to the splicing defect, with some genes showing up- or downregulation, while most did not change significantly. The observed residual U12-type splicing activity could be explained with the mutant U6atac allele having a low level of catalytic activity. Detailed analysis of all genes suggested that a defect in the splicing of the U12-type intron of the mitochondrial prohibitin gene may be the primary cause of the various downstream effects detected in the microarray analysis.
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