ArticleJournal of neurochemistry2013
A HuD-ZBP1 ribonucleoprotein complex localizes GAP-43 mRNA into axons through its 3' untranslated region AU-rich regulatory element.
Article in Journal of neurochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 81 citations in OpenAlex.
- ELAVL Proteins, miRNA Fate, and Extracellular RNA Communication in Brain Aging and Neurodegeneration.Cells · 2026Review
- 3'UTR regulation of axon translation and optic nerve regeneration.Molecular neurodegeneration · 2026Article
- Dynamic subtype- and context-specific subcellular RNA regulation in growth cones of developing neurons of the cerebral cortex.Nature neuroscience · 2026Article
- CYFIP1 governs the development of cortical axons by modulating calcium availability.Nature communications · 2025Article
- KHSRP-mediated decay of axonally localized prenyl-Cdc42 mRNA slows nerve regeneration.PLoS genetics · 2025Article
- HuD impairs neuromuscular junctions and induces apoptosis in human iPSC and Drosophila ALS models.Nature communications · 2024Article
- Posttranscriptional Regulation of Gene Expression Participates in the Myelin Restoration in Mouse Models of Multiple Sclerosis: Antisense Modulation of HuR and HuD ELAV RNA Binding Protein.Molecular neurobiology · 2023Article
- From form to function: mAdvances in biological regulation · 2023Review
- Emerging Roles for the RNA-Binding Protein HuD (ELAVL4) in Nervous System Diseases.International journal of molecular sciences · 2022Review
- KHSRP loss increases neuronal growth and synaptic transmission and alters memory consolidation through RNA stabilization.Communications biology · 2022Article
- Intra-axonal translation of Khsrp mRNA slows axon regeneration by destabilizing localized mRNAs.Nucleic acids research · 2022Article
- RNA and neuronal function: the importance of post-transcriptional regulation.Oxford open neuroscience · 2022Review
- Axonal mRNA localization and translation: local events with broad roles.Cellular and molecular life sciences : CMLS · 2021Review
- ALS-related FUS mutations alter axon growth in motoneurons and affect HuD/ELAVL4 and FMRP activity.Communications biology · 2021Article
- Review
- Cytoplasmic cleavage of IMPA1 3' UTR is necessary for maintaining axon integrity.Cell reports · 2021Article
- The functional organization of axonal mRNA transport and translation.Nature reviews. Neuroscience · 2021Review
- Regulation of Fetal Genes by Transitions among RNA-Binding Proteins during Liver Development.International journal of molecular sciences · 2020Article
- Molecular mechanisms behind mRNA localization in axons.Open biology · 2020Review
- Intra-axonal mechanisms driving axon regeneration.Brain research · 2020Review
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
Localized translation of axonal mRNAs contributes to developmental and regenerative axon growth. Although untranslated regions (UTRs) of many different axonal mRNAs appear to drive their localization, there has been no consensus RNA structure responsible for this localization. We recently showed that limited expression of ZBP1 protein restricts axonal localization of both β-actin and GAP-43 mRNAs. β-actin 3'UTR has a defined element for interaction with ZBP1, but GAP-43 mRNA shows no homology to this RNA sequence. Here, we show that an AU-rich regulatory element (ARE) in GAP-43's 3'UTR is necessary and sufficient for its axonal localization. Axonal GAP-43 mRNA levels increase after in vivo injury, and GAP-43 mRNA shows an increased half-life in regenerating axons. GAP-43 mRNA interacts with both HuD and ZBP1, and HuD and ZBP1 co-immunoprecipitate in an RNA-dependent fashion. Reporter mRNA with the GAP-43 ARE competes with endogenous β-actin mRNA for axonal localization and decreases axon length and branching similar to the β-actin 3'UTR competing with endogenous GAP-43 mRNA. Conversely, over-expressing GAP-43 coding sequence with its 3'UTR ARE increases axonal elongation and this effect is lost when just the ARE is deleted from GAP-43's 3'UTR. We have recently found that over-expression of GAP-43 using an axonally targeted construct with the 3'UTRs of GAP-43 promoted elongating growth of axons, while restricting the mRNA to the cell body with the 3'UTR of γ-actin had minimal effect on axon length. In this study, we show that the ARE in GAP-43's 3'UTR is responsible for localization of GAP-43 mRNA into axons and is sufficient for GAP-43 protein's role in elongating axonal growth.
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