ArticleNeurobiology of disease2023
Dissecting the roles of EIF4G homologs reveals DAP5 as a modifier of CGG repeat-associated toxicity in a Drosophila model of FXTAS.
Article in Neurobiology of disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Inter-individual differentially methylated region-targeted EWAS reveals epigenetic signatures of early childhood adversity.Epigenomics · 2026Article
- eVGeMdb: a manually curated database for experimentally validated genetic modifiers of neurodegenerative disorders.NAR molecular medicine · 2026Article
- Lacosamide Interaction with Expanded CGG Repeats RNA and Its Role in Modulating Poly-Glycine Protein-Mediated Toxicity in Fragile‑X Tremor/Ataxia Syndrome.ACS pharmacology & translational science · 2025Article
- Tyrosine Peptides Alleviates Multifaceted Toxicity Linked to Expanded CGG Repeats in Fragile X‑Associated Tremor/Ataxia Syndrome.ACS pharmacology & translational science · 2025Article
- Advances on the Mechanisms and Therapeutic Strategies in Non-coding CGG Repeat Expansion Diseases.Molecular neurobiology · 2024Review
- Decoding Nucleotide Repeat Expansion Diseases: Novel Insights fromInternational journal of molecular sciences · 2024Review
- Lost in Translation: When the Rules Do Not Apply.Wiley interdisciplinary reviews. RNAReview
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Neurodegeneration in Fragile X-associated tremor/ataxia syndrome (FXTAS) is caused by a CGG trinucleotide repeat expansion in the 5' UTR of FMR1. Expanded CGG repeat RNAs form stable secondary structures, which in turn support repeat-associated non-AUG (RAN) translation to produce toxic peptides. The parameters that impact RAN translation initiation efficiency are not well understood. Here we used a Drosophila melanogaster model of FXTAS to evaluate the role of the eIF4G family of eukaryotic translation initiation factors (EIF4G1, EIF4GII and EIF4G2/DAP5) in modulating RAN translation and CGG repeat-associated toxicity. DAP5 knockdown robustly suppressed CGG repeat-associated toxicity and inhibited RAN translation. Furthermore, knockdown of initiation factors that preferentially associate with DAP5 (such as EIF2β, EIF3F and EIF3G) also selectively suppressed CGG repeat-induced eye degeneration. In mammalian cellular reporter assays, DAP5 knockdown exhibited modest and cell-type specific effects on RAN translation. Taken together, these data support a role for DAP5 in CGG repeat associated toxicity possibly through modulation of RAN translation.
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