Srsf1 and Elavl1 act antagonistically on neuronal fate choice in the developing neocortex by controlling TrkC receptor isoform expression
- PMID: 37697438
- PMCID: PMC10602877
- DOI: 10.1093/nar/gkad703
Srsf1 and Elavl1 act antagonistically on neuronal fate choice in the developing neocortex by controlling TrkC receptor isoform expression
Erratum in
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Correction to 'Srsf1 and Elavl1 act antagonistically on neuronal fate choice in the developing neocortex by controlling TrkC receptor isoform expression'.Nucleic Acids Res. 2024 Feb 9;52(3):1522. doi: 10.1093/nar/gkad1238. Nucleic Acids Res. 2024. PMID: 38142458 Free PMC article. No abstract available.
Abstract
The seat of higher-order cognitive abilities in mammals, the neocortex, is a complex structure, organized in several layers. The different subtypes of principal neurons are distributed in precise ratios and at specific positions in these layers and are generated by the same neural progenitor cells (NPCs), steered by a spatially and temporally specified combination of molecular cues that are incompletely understood. Recently, we discovered that an alternatively spliced isoform of the TrkC receptor lacking the kinase domain, TrkC-T1, is a determinant of the corticofugal projection neuron (CFuPN) fate. Here, we show that the finely tuned balance between TrkC-T1 and the better known, kinase domain-containing isoform, TrkC-TK+, is cell type-specific in the developing cortex and established through the antagonistic actions of two RNA-binding proteins, Srsf1 and Elavl1. Moreover, our data show that Srsf1 promotes the CFuPN fate and Elavl1 promotes the callosal projection neuron (CPN) fate in vivo via regulating the distinct ratios of TrkC-T1 to TrkC-TK+. Taken together, we connect spatio-temporal expression of Srsf1 and Elavl1 in the developing neocortex with the regulation of TrkC alternative splicing and transcript stability and neuronal fate choice, thus adding to the mechanistic and functional understanding of alternative splicing in vivo.
© The Author(s) 2023. Published by Oxford University Press on behalf of Nucleic Acids Research.
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Correction to 'Srsf1 and Elavl1 act antagonistically on neuronal fate choice in the developing neocortex by controlling TrkC receptor isoform expression'.Nucleic Acids Res. 2024 Feb 9;52(3):1522. doi: 10.1093/nar/gkad1238. Nucleic Acids Res. 2024. PMID: 38142458 Free PMC article. No abstract available.
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References
-
- Florio M., Huttner W.B. Neural progenitors, neurogenesis and the evolution of the neocortex. Dev. Camb. Engl. 2014; 141:2182–2194. - PubMed
-
- Kriegstein A., Noctor S., Martínez-Cerdeño V. Patterns of neural stem and progenitor cell division may underlie evolutionary cortical expansion. Nat. Rev. Neurosci. 2006; 7:883–890. - PubMed
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