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Srsf1 and Elavl1 act antagonistically on neuronal fate choice in the developing neocortex by controlling TrkC receptor isoform expression.
Weber, A Ioana; Parthasarathy, Srinivas; Borisova, Ekaterina; Epifanova, Ekaterina; Preußner, Marco; Rusanova, Alexandra; Ambrozkiewicz, Mateusz C; Bessa, Paraskevi; Newman, Andrew G; Müller, Lisa; Schaal, Heiner; Heyd, Florian; Tarabykin, Victor.
Afiliación
  • Weber AI; Charité Universitätsmedizin Berlin, Institute of Cell Biology and Neurobiology, Charitéplatz 1, 10117 Berlin, Germany.
  • Parthasarathy S; Freie Universität Berlin, Institute of Chemistry and Biochemistry, Takustr. 6, 14195, Berlin, Germany.
  • Borisova E; Charité Universitätsmedizin Berlin, Institute of Cell Biology and Neurobiology, Charitéplatz 1, 10117 Berlin, Germany.
  • Epifanova E; Charité Universitätsmedizin Berlin, Institute of Cell Biology and Neurobiology, Charitéplatz 1, 10117 Berlin, Germany.
  • Preußner M; Research Institute of Medical Genetics, Tomsk National Research Medical Center of the Russian Academy of Sciences, 634009, Tomsk, Russia.
  • Rusanova A; Charité Universitätsmedizin Berlin, Institute of Cell Biology and Neurobiology, Charitéplatz 1, 10117 Berlin, Germany.
  • Ambrozkiewicz MC; Institute of Neuroscience, Lobachevsky State University of Nizhny Novgorod, 603950, Nizhny Novgorod Oblast, Russia.
  • Bessa P; Freie Universität Berlin, Institute of Chemistry and Biochemistry, Takustr. 6, 14195, Berlin, Germany.
  • Newman AG; Charité Universitätsmedizin Berlin, Institute of Cell Biology and Neurobiology, Charitéplatz 1, 10117 Berlin, Germany.
  • Müller L; Research Institute of Medical Genetics, Tomsk National Research Medical Center of the Russian Academy of Sciences, 634009, Tomsk, Russia.
  • Schaal H; Charité Universitätsmedizin Berlin, Institute of Cell Biology and Neurobiology, Charitéplatz 1, 10117 Berlin, Germany.
  • Heyd F; Charité Universitätsmedizin Berlin, Institute of Cell Biology and Neurobiology, Charitéplatz 1, 10117 Berlin, Germany.
  • Tarabykin V; Charité Universitätsmedizin Berlin, Institute of Cell Biology and Neurobiology, Charitéplatz 1, 10117 Berlin, Germany.
Nucleic Acids Res ; 51(19): 10218-10237, 2023 10 27.
Article en En | MEDLINE | ID: mdl-37697438
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.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neocórtex / Receptor trkC Límite: Animals Idioma: En Revista: Nucleic Acids Res Año: 2023 Tipo del documento: Article País de afiliación: Alemania

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neocórtex / Receptor trkC Límite: Animals Idioma: En Revista: Nucleic Acids Res Año: 2023 Tipo del documento: Article País de afiliación: Alemania
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