ArticleNature structural & molecular biology2025
Core splicing architecture and early spliceosomal recognition determine microexon sensitivity to SRRM3/4.
Article in Nature structural & molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
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Who cites it
3 citing papers in PubMed.
- Efficient co-transcriptional splicing enforces rapid microexon definition and inclusion by SRRM4.bioRxiv : the preprint server for biology · 2026Article
- Ethanol selectively disrupts neuronal microexon regulation and chromatin marks in PC12 cells.Frontiers in cellular neuroscience · 2026Article
- Phenotypic impact of individual conserved neuronal microexons and their master regulators in zebrafish.eLife · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microexons are essential for the proper operation of neurons and pancreatic endocrine cells, in which their inclusion depends on the splicing factors SRRM3 and SRRM4 (SRRM3/4). However, in pancreatic cells, lower expression of these regulators limits inclusion to only the most sensitive subset among all neuronal microexons. Although various cis-acting elements can contribute to microexon regulation, how they determine this differential dose response and the corresponding high or low sensitivity to SRRM3/4 remains unknown. Here we use massively parallel splicing assays probing 28,535 variants to show that sensitivity to SRRM4 is conserved across vertebrates. Our data support a regulatory model whereby high or low microexon sensitivity is largely determined by the interplay between core splicing architecture and length constraints. This conclusion is further supported by distinct spliceosome activities in the absence of SRRM3/4 and by a mathematical model that assumes that the two types of microexons differ only in their efficiency to recruit early spliceosomal components.
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Registered trials
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