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Translational derepression of Elavl4 isoforms at their alternative 5′ UTRs determines neuronal development

MPG-Autoren
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Kraushar,  Matthew
High-Resolution Neurogenetics (Matthew Kraushar), Dept. of Genome Regulation (Head: Alexander Meissner), Max Planck Institute for Molecular Genetics, Max Planck Society;
Department of Neuroscience and Cell Biology, Rutgers University, Robert Wood Johnson Medical School, Piscataway, NJ, 08854, USA;
Graduate Program in Neurosciences, Rutgers University, Piscataway, NJ, 08854, USA;

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Zitation

Popovitchenko, T., Park, Y., Page, N. F., Luo, X., Krsnik, Z., Liu, Y., et al. (2020). Translational derepression of Elavl4 isoforms at their alternative 5′ UTRs determines neuronal development. Nature Communications, 11(1): 1674. doi:10.1038/s41467-020-15412-8.


Zitierlink: https://hdl.handle.net/21.11116/0000-000A-7A5A-9
Zusammenfassung
Neurodevelopment requires precise regulation of gene expression, including post-transcriptional regulatory events such as alternative splicing and mRNA translation. However, translational regulation of specific isoforms during neurodevelopment and the mechanisms behind it remain unknown. Using RNA-seq analysis of mouse neocortical polysomes, here we report translationally repressed and derepressed mRNA isoforms during neocortical neurogenesis whose orthologs include risk genes for neurodevelopmental disorders. We demonstrate that the translation of distinct mRNA isoforms of the RNA binding protein (RBP), Elavl4, in radial glia progenitors and early neurons depends on its alternative 5' UTRs. Furthermore, 5' UTR-driven Elavl4 isoform-specific translation depends on upstream control by another RBP, Celf1. Celf1 regulation of Elavl4 translation dictates development of glutamatergic neurons. Our findings reveal a dynamic interplay between distinct RBPs and alternative 5' UTRs in neuronal development and underscore the risk of post-transcriptional dysregulation in co-occurring neurodevelopmental disorders.