ArticleCommunications biology2018
Conserved Pbp1/Ataxin-2 regulates retrotransposon activity and connects polyglutamine expansion-driven protein aggregation to lifespan-controlling rDNA repeats.
Article in Communications biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Review
- Epigenetic pharmacology in aging: from mechanisms to therapies for age-related disorders.Frontiers in pharmacology · 2025Review
- Repetitive elements in aging and neurodegeneration.Trends in genetics : TIG · 2023Review
- Ataxin-2 gene: a powerful modulator of neurological disorders.Current opinion in neurology · 2021Review
- Biomolecular condensates as arbiters of biochemical reactions inside the nucleus.Communications biology · 2020Review
- RNA-cDNA hybrids mediate transposition via different mechanisms.Scientific reports · 2020Article
- Roles for Non-coding RNAs in Spatial Genome Organization.Frontiers in cell and developmental biology · 2019Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ribosomal DNA (rDNA) repeat instability and protein aggregation are thought to be two major and independent drivers of cellular aging. Pbp1, the yeast ortholog of human ATXN2, maintains rDNA repeat stability and lifespan via suppression of RNA-DNA hybrids. ATXN2 polyglutamine expansion drives neurodegeneration causing spinocerebellar ataxia type 2 and promoting amyotrophic lateral sclerosis. Here, molecular characterization of Pbp1 revealed that its knockout or subjection to disease-modeling polyQ expansion represses Ty1 (Transposons of Yeast) retrotransposons by respectively promoting Trf4-depedendent RNA turnover and Ty1 Gag protein aggregation. This aggregation, but not its impact on retrotransposition, compromises rDNA repeat stability and shortens lifespan by hyper-activating Trf4-dependent turnover of intergenic ncRNA within the repeats. We uncover a function for the conserved Pbp1/ATXN2 proteins in the promotion of retrotransposition, create and describe powerful yeast genetic models of ATXN2-linked neurodegenerative diseases, and connect the major aging mechanisms of rDNA instability and protein aggregation.
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Registered trials
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