ArticleDevelopmental biology2012
Eif4a3 is required for accurate splicing of the Xenopus laevis ryanodine receptor pre-mRNA.
Article in Developmental biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- EIF4A3-Induced Circular RNA CircDdb1 Promotes Muscle Atrophy through Encoding a Novel Protein CircDdb1-867aa.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The exon junction complex is required for DMD gene splicing fidelity and myogenic differentiation.Cellular and molecular life sciences : CMLS · 2024Article
- An exon junction complex-independent function of Barentsz in neuromuscular synapse growth.EMBO reports · 2022Article
- Zebrafish rbm8a and magoh mutants reveal EJC developmental functions and new 3'UTR intron-containing NMD targets.PLoS genetics · 2020Article
- Article
- SOX9 has distinct regulatory roles in alternative splicing and transcription.Nucleic acids research · 2018Article
- EIF4A3 deficient human iPSCs and mouse models demonstrate neural crest defects that underlie Richieri-Costa-Pereira syndrome.Human molecular genetics · 2017Article
- Haploinsufficiency for Core Exon Junction Complex Components Disrupts Embryonic Neurogenesis and Causes p53-Mediated Microcephaly.PLoS genetics · 2016Article
- The exon junction complex as a node of post-transcriptional networks.Nature reviews. Molecular cell biology · 2016Review
- The exon junction complex controls transposable element activity by ensuring faithful splicing of the piwi transcript.Genes & development · 2014Article
- Transcriptome-wide modulation of splicing by the exon junction complex.Genome biology · 2014Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The Exon Junction Complex (EJC) plays a critical role in multiple posttranscriptional events, including RNA subcellular localization, nonsense-mediated decay (NMD), and translation. We previously reported that knockdown of the EJC core component Eukaryotic initiation factor 4a3 (Eif4a3) results in full-body paralysis of embryos of the frog, Xenopus laevis. Here, we explore the cellular and molecular mechanisms underlying this phenotype. We find that cultured muscle cells derived from Eif4a3 morphants do not contract, and fail to undergo calcium-dependent calcium release in response to electrical stimulation or treatment with caffeine. We show that ryr (ryanodine receptor) transcripts are incorrectly spliced in Eif4a3 morphants, and demonstrate that inhibition of Xenopus Ryr function similarly results in embryonic paralysis. These results suggest that the EJC mediates muscle cell function via regulation of pre-mRNA splicing during early vertebrate embryogenesis.
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