ArticleFEMS yeast research2018
Yeast screen for modifiers of C9orf72 poly(glycine-arginine) dipeptide repeat toxicity.
Article in FEMS yeast research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Effects of heterologous human tau protein expression in yeast models of proteotoxic stress response.CNS neuroscience & therapeutics · 2024Article
- CRISPR screen for protein inclusion formation uncovers a role for SRRD in the regulation of intermediate filament dynamics and aggresome assembly.PLoS genetics · 2024Article
- Redox dysregulation as a driver for DNA damage and its relationship to neurodegenerative diseases.Translational neurodegeneration · 2023Review
- C9orf72 dipeptides disrupt the nucleocytoplasmic transport machinery and cause TDP-43 mislocalisation to the cytoplasm.Scientific reports · 2022Article
- The progress inSmall GTPases · 2022Review
- Epigenetic Small Molecules Rescue Nucleocytoplasmic Transport and DNA Damage Phenotypes in C9ORF72 ALS/FTD.Brain sciences · 2021Article
- The nuclear ubiquitin ligase adaptor SPOP is a conserved regulator of C9orf72 dipeptide toxicity.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Widespread displacement of DNA- and RNA-binding factors underlies toxicity of arginine-rich cell-penetrating peptides.The EMBO journal · 2021Article
- Gene co-expression network analysis in human spinal cord highlights mechanisms underlying amyotrophic lateral sclerosis susceptibility.Scientific reports · 2021Article
- Nucleolin Rescues TDP-43 Toxicity in Yeast and Human Cell Models.Frontiers in cellular neuroscience · 2021Article
- Altered Phase Separation and Cellular Impact inFrontiers in cellular neuroscience · 2021Article
- Nucleo-cytoplasmic transport defects and protein aggregates in neurodegeneration.Translational neurodegeneration · 2020Review
- Traffic jam at the nuclear pore: All roads lead to nucleocytoplasmic transport defects in ALS/FTD.Neurobiology of disease · 2020Review
- Mutant C9orf72 human iPSC-derived astrocytes cause non-cell autonomous motor neuron pathophysiology.Glia · 2020Article
- Article
- Application of yeast to studying amyloid and prion diseases.Advances in genetics · 2020Review
- Emerging Evidence Highlighting the Importance of Redox Dysregulation in the Pathogenesis of Amyotrophic Lateral Sclerosis (ALS).Frontiers in cellular neuroscience · 2020Article
- Extensive transcriptomic study emphasizes importance of vesicular transport in C9orf72 expansion carriers.Acta neuropathologica communications · 2019Article
- Repeat-Associated Non-ATG Translation: Molecular Mechanisms and Contribution to Neurological Disease.Annual review of neuroscience · 2019Review
- Toxic expanded GGGGCC repeat transcription is mediated by the PAF1 complex in C9orf72-associated FTD.Nature neuroscience · 2019Article
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2 authors.
Funding
Abstract
A hexanucleotide repeat expansion in the C9orf72 gene has been identified as the most common cause of amyotrophic lateral sclerosis and frontotemporal dementia. The expanded hexanucleotide repeat is translated by an unconventional mechanism to produce five species of dipeptide repeat (DPR) proteins, glycine-proline (GP), glycine-alanine (GA), glycine-arginine (GR), proline-alanine (PA) and proline-arginine (PR). Of these, the arginine-rich ones, PR and GR, are highly toxic in a variety of model systems, ranging from human cells, to Drosophila, to even the budding yeast, Saccharomyces cerevisiae. We recently performed a genetic screen in yeast for modifiers of PR toxicity and identified suppressors and enhancers, many of which function in nucleocytoplasmic transport. Whether or not GR toxicity involves similar mechanisms to PR is unresolved. Therefore, we performed a genetic screen in yeast to identify modifiers of GR toxicity and compared the results of the GR screen to results from our previous PR screen. Surprisingly, there was only a small degree of overlap between the two screens, suggesting potential for distinct toxicity mechanisms between PR and GR.
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