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- W4308791859 abstract "Emerging evidence suggests that intron-detaining transcripts (IDTs) are a nucleus-detained and polyadenylated mRNA pool for cell to quickly and effectively respond to environmental stimuli and stress. However, the underlying mechanisms of detained intron (DI) splicing are still largely unknown. Here, we suggest that post-transcriptional DI splicing is paused at the Bact state, an active spliceosome but not catalytically primed, which depends on Smad Nuclear Interacting Protein 1 (SNIP1) and RNPS1 (a serine-rich RNA binding protein) interaction. RNPS1 and Bact components preferentially dock at DIs and the RNPS1 docking is sufficient to trigger spliceosome pausing. Haploinsufficiency of Snip1 attenuates neurodegeneration and globally rescues IDT accumulation caused by a previously reported mutant U2 snRNA, a basal spliceosomal component. Snip1 conditional knockout in the cerebellum decreases DI splicing efficiency and causes neurodegeneration. Therefore, we suggest that SNIP1 and RNPS1 form a molecular brake to promote spliceosome pausing, and that its misregulation contributes to neurodegeneration." @default.
- W4308791859 created "2022-11-15" @default.
- W4308791859 creator A5008301692 @default.
- W4308791859 creator A5037303783 @default.
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- W4308791859 creator A5061579496 @default.
- W4308791859 creator A5079587373 @default.
- W4308791859 creator A5079974007 @default.
- W4308791859 date "2022-11-11" @default.
- W4308791859 modified "2023-10-16" @default.
- W4308791859 title "A molecular brake that modulates spliceosome pausing at detained introns contributes to neurodegeneration" @default.
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