ArticleCell reports2025
mRNA decay pre-complex assembly drives timely cell-state transitions during differentiation.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed.
- The RNA-binding activity of theRNA biology · 2026Article
- Stem cells as an essential mediator of the exercise-tumorigenesis link.Nature reviews. Cancer · 2026Review
- RNA-binding is the essential biological function of thebioRxiv : the preprint server for biology · 2026Article
- Host-Driven Functional Divergence in Gut Microbiota of Honeybees Apis cerana and Apis mellifera: Implications for Pollination, Nutrition, and Sustainable Apiculture.Current microbiology · 2025Article
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Abstract
Complexes that control mRNA stability and translation promote timely cell-state transitions during differentiation by ensuring appropriate expression patterns of key developmental regulators. The Drosophila RNA-binding protein brain tumor (Brat) promotes the degradation of target transcripts during the maternal-to-zygotic transition in syncytial embryos and uncommitted intermediate neural progenitors (immature INPs). We identify ubiquitin-specific protease 5 (Usp5) as a candidate Brat interactor essential for the degradation of Brat target mRNAs. Usp5 promotes the formation of the Brat-deadenylase pre-complex in mitotic neural stem cells (neuroblasts) by facilitating Brat interactions with the scaffolding components of deadenylase complexes. The adaptor protein Miranda binds the RNA-binding domain of Brat, limiting its ability to bind target mRNAs in mitotic neuroblasts. Cortical displacement of Miranda activates Brat-deadenylase complex activity in immature INPs. We propose that the assembly of an enzymatically inactive and RNA-binding-deficient pre-complex poises mRNA degradation machineries for rapid activation, driving timely developmental transitions.
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