Translational regulation of Sf1 integrates alternative splicing and hematopoietic stem cell fate.
- Open access
Translational regulation of Sf1 via a conserved 5' UTR modulates hematopoietic stem cell fate by controlling spliceosome activity and gene splicing.
- Why it matters: Understanding how post-transcriptional mechanisms influence HSC differentiation fills a critical gap in stem cell biology and could inform regenerative medicine strategies.
- What they did: The study used activity-based signatures of 305 splicing regulators and identified Sf1 as a key translational control point, regulated by its structured 5' UTR and Igf2bp2, affecting cell fate decisions.
- The result: Disrupting Sf1 translation shifts differentiation toward stem and erythroid lineages, alters alternative splicing of important genes, and impacts DNA damage response, revealing a new layer of HSC regulation.