ArticleAging cell2017
The replicative lifespan-extending deletion of SGF73 results in altered ribosomal gene expression in yeast.
Article in Aging cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- UPS writes a new saga of SAGA.Biochimica et biophysica acta. Gene regulatory mechanisms · 2023Review
- Tra1 controls the transcriptional landscape of the aging cell.G3 (Bethesda, Md.) · 2023Article
- Transcriptional control of ribosome biogenesis in yeast: links to growth and stress signals.Biochemical Society transactions · 2021Review
- Nitrogen starvation reveals the mitotic potential of mutants in the S/MAPK pathways.Nature communications · 2020Article
- Gene Deregulation and Underlying Mechanisms in Spinocerebellar Ataxias With Polyglutamine Expansion.Frontiers in neuroscience · 2020Review
- Molecular Targets and Therapeutic Strategies in Spinocerebellar Ataxia Type 7.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
- Divergent Aging of Isogenic Yeast Cells Revealed through Single-Cell Phenotypic Dynamics.Cell systems · 2019Article
- Connecting GCN5's centromeric SAGA to the mitotic tension-sensing checkpoint.Molecular biology of the cell · 2018Article
- The evolutionarily conserved factor Sus1/ENY2 plays a role in telomere length maintenance.Current genetics · 2018Article
- Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Sgf73, a core component of SAGA, is the yeast orthologue of ataxin-7, which undergoes CAG-polyglutamine repeat expansion leading to the human neurodegenerative disease spinocerebellar ataxia type 7 (SCA7). Deletion of SGF73 dramatically extends replicative lifespan (RLS) in yeast. To further define the basis for Sgf73-mediated RLS extension, we performed ChIP-Seq, identified 388 unique genomic regions occupied by Sgf73, and noted enrichment in promoters of ribosomal protein (RP)-encoding genes. Of 388 Sgf73 binding sites, 33 correspond to 5' regions of genes implicated in RLS extension, including 20 genes encoding RPs. Furthermore, half of Sgf73-occupied, RLS-linked RP genes displayed significantly reduced expression in sgf73Δ mutants, and double null strains lacking SGF73 and a Sgf73-regulated, RLS-linked RP gene exhibited no further increase in replicative lifespan. We also found that sgf73Δ mutants display altered acetylation of Ifh1, an important regulator of RP gene transcription. These findings implicate altered ribosomal protein expression in sgf73Δ yeast RLS and highlight altered acetylation as a pathway of relevance for SCA7 neurodegeneration.
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Registered trials
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.