The predicted RNA-binding protein ETR-1/CELF1 acts in muscles to regulate neuroblast migration inCaenorhabditis elegans
| Autor: | Matthew E Ochs, Erik A. Lundquist, Matthew P. Josephson |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
q neuroblast
RNA-binding protein QH426-470 migration 03 medical and health sciences Exon 0302 clinical medicine Neuroblast migration Genetics Molecular Biology Genetics (clinical) Caenorhabditis elegans 030304 developmental biology 0303 health sciences Gene knockdown biology c. elegans Alternative splicing Wnt signaling pathway crispr-seq biology.organism_classification etr-1 Cell biology celf1 030217 neurology & neurosurgery Genetic screen |
| Zdroj: | G3: Genes, Genomes, Genetics, Vol 10, Iss 7, Pp 2365-2376 (2020) |
| Popis: | SummaryNeuroblast migration is a critical aspect of nervous system development (e.g., neural crest migration). In an unbiased forward genetic screen, we identified a novel player in neuroblast migration, the ETR-1/CELF1 RNA binding protein. CELF1 RNA binding proteins are involved in multiple aspects of RNA processing including alternative splicing, stability, and translation. We find that a specific mutation in alternatively-spliced exon 8 results in migration defects of the AQR and PQR neurons, and not the embryonic lethality and body wall muscle defects of complete knockdown of the locus. Surprisingly, ETR-1 was required in body wall muscle cells for AQR/PQR migration (i.e. it acts cell non-autonomously). Genetic interactions indicate that ETR-1 acts with Wnt signaling, either in the Wnt pathway or in a parallel pathway. Possibly, ETR-1 is involved in the production of a Wnt signal or a parallel signal by the body wall muscles that controls AQR and PQR neuronal migration. In humans, CELF1 is involved in a number of neuromuscular disorders. If the role of ETR-1/CELF1 is conserved, these disorders might also involve cell or neuronal migration. Finally, we describe a technique of amplicon sequencing to detect rare, cell-specific genome edits by CRISPR/Cas9in vivo(CRISPR-seq) as an alternative to the T7E1 assay. |
| Databáze: | OpenAIRE |
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