ArticleRNA biology2013
Regulation of Dscam exon 17 alternative splicing by steric hindrance in combination with RNA secondary structures.
Article in RNA biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Regulatory paradigm of Dscam1 stochastic alternative splicing through conserved long-range RNA structures.Nucleic acids research · 2026Article
- Synthesis of fluorescence labelled aptamers for use as low-cost reagents in HIV/AIDS research and diagnostics.Biomedical reports · 2022Article
- Restriction of an intron size en route to endothermy.Nucleic acids research · 2021Article
- isoTarget: A Genetic Method for Analyzing the Functional Diversity of Splicing Isoforms In Vivo.Cell reports · 2020Article
- Revisiting Dscam diversity: lessons from clustered protocadherins.Cellular and molecular life sciences : CMLS · 2019Review
- Article
- Review
- Role and convergent evolution of competing RNA secondary structures in mutually exclusive splicing.RNA biology · 2017Article
- 14-3-3 isoforms bind directly exon B of the 5'-UTR of human surfactant protein A2 mRNA.American journal of physiology. Lung cellular and molecular physiology · 2015Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The gene Down syndrome cell adhesion molecule (Dscam) potentially encodes 38 016 distinct isoforms in Drosophila melanogaster via mutually exclusive splicing. Here we reveal a combinatorial mechanism of regulation of Dscam exon 17 mutually exclusive splicing through steric hindrance in combination with RNA secondary structure. This mutually exclusive behavior is enforced by steric hindrance, due to the close proximity of the exon 17.2 branch point to exon 17.1 in Diptera, and the interval size constraint in non-Dipteran species. Moreover, intron-exon RNA structures are evolutionarily conserved in 36 non-Drosophila species of six distantly related orders (Diptera, Lepidoptera, Coleoptera, Hymenoptera, Hemiptera, and Phthiraptera), which regulates the selection of exon 17 variants via masking the splice site. By contrast, a previously uncharacterized RNA structure specifically activated exon 17.1 by bringing splice sites closer together in Drosophila, while the other moderately suppressed exon 17.1 selection by hindering the accessibility of polypyrimidine sequences. Taken together, these data suggest a phylogeny of increased complexity in regulating alternative splicing of Dscam exon 17 spanning more than 300 million years of insect evolution. These results also provide models of the regulation of alternative splicing through steric hindrance in combination with dynamic structural codes.
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