ArticleHuman molecular genetics2013
Distinct roles for Toll and autophagy pathways in double-stranded RNA toxicity in a Drosophila model of expanded repeat neurodegenerative diseases.
Article in Human molecular genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Autophagy at the Crossroads of Protein and RNA Toxicity in Repeat Expansion Cerebellar Ataxias.Cells · 2026Review
- The molecular toll pathway repertoire in anopheline mosquitoes.Developmental and comparative immunology · 2025Article
- The Molecular Toll Pathway Repertoire in Anopheline Mosquitoes.bioRxiv : the preprint server for biology · 2024Article
- Partners in crime: Proteins implicated in RNA repeat expansion diseases.Wiley interdisciplinary reviews. RNA · 2022Review
- ALS-associated genes in SCA2 mouse spinal cord transcriptomes.Human molecular genetics · 2020Article
- Neurodegenerative diseases have genetic hallmarks of autoinflammatory disease.Human molecular genetics · 2018Review
- Rapidly Evolving Toll-3/4 Genes Encode Male-Specific Toll-Like Receptors in Drosophila.Molecular biology and evolution · 2017Article
- The Enemy within: Innate Surveillance-Mediated Cell Death, the Common Mechanism of Neurodegenerative Disease.Frontiers in neuroscience · 2016Article
- The role of the immune system in triplet repeat expansion diseases.Mediators of inflammation · 2015Review
- The RNA-centred view of the synapse: non-coding RNAs and synaptic plasticity.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Review
- Innate immune activation in neurodegenerative disease.Nature reviews. Immunology · 2014Review
- Autophagy in Drosophila: from historical studies to current knowledge.BioMed research international · 2014Review
- RNA pathogenesis via Toll-like receptor-activated inflammation in expanded repeat neurodegenerative diseases.Frontiers in molecular neuroscience · 2013Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
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Abstract
Dominantly inherited expanded repeat neurodegenerative diseases are caused by the expansion of variable copy number tandem repeat sequences in otherwise unrelated genes. Some repeats encode polyglutamine that is thought to be toxic; however, other repeats do not encode polyglutamine indicating either multiple pathogenic pathways or an alternative common toxic agent. As these diseases share numerous clinical features and expanded repeat RNA is a common intermediary, RNA-based pathogenesis has been proposed, based on its toxicity in animal models. In Drosophila, double-stranded (rCAG.rCUG∼100) RNA toxicity is Dicer dependent and generates single-stranded (rCAG)7, an entity also detected in affected Huntington's Disease (HD) brains. We demonstrate that Drosophila rCAG.rCUG∼100 RNA toxicity perturbs several pathways including innate immunity, consistent with the observation in HD that immune activation precedes neuronal toxicity. Our results show that Drosophila rCAG.rCUG∼100 RNA toxicity is dependent upon Toll signaling and sensitive to autophagy, further implicating innate immune activation. In exhibiting molecular and cellular hallmarks of HD, double-stranded RNA-mediated activation of innate immunity is, therefore, a candidate pathway for this group of human genetic diseases.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.