Redistribution of silencing proteins from telomeres to the nucleolus is associated with extension of life span in S. cerevisiae
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A prior genetic study indicated that activity of Sir silencing proteins at a hypothetical AGE locus is essential for long life span. In this model, the SIR4-42 mutation would direct the Sir protein complex to the AGE locus, giving rise to a long life span. We show by indirect immunofluorescence that Sir3p and Sir4p are redirected to the nucleolus in the SIR4-42 mutant. Furthermore, this relocalization is dependent on both UTH4 a novel yeast gene that extends life span, and its homologue YGL023. Strikingly, the Sir complex is relocalized from telomeres to the nucleolus in old wild-type cells. We propose that the rDNA is the AGE locus and that nucleolar function is compromised in old yeast cells in a way that may be mitigated by targeting of Sir proteins to the nucleolus.
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Relocalization of chromatin factors to repair sites keeps cells in survival mode until repair finishes.
“The benefit is that the relocalization of chromatin factors to sites of repair places cells in survival mode until repair is complete (Kennedy et al., 1997; Mills et al., 1999; Oberdoerffer et al., 2008; Sinclair and LaPlante, 2019; Smeal et al., 1996).”
From Loss of epigenetic information as a cause of mammalian aging (2023) · cites this paper as Kennedy et al., 1997
The Discussion (page unavailable in our copy) reports that Sir silencing proteins move from telomeres to the nucleolus in old yeast cells and associates increased nucleolar Sir activity with longer life span. It does not establish that they move to repair sites or keep cells in a survival mode until repair is complete. (LLM, conf=0.82)
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Self-citation
- Authors
- Kennedy, B. K., Gotta, M., Sinclair, D. A., Mills, K., McNabb, D. S., Murthy, M., Pak, S. M., Laroche, T., Gasser, S. M., & Guarente, L.
- Affiliations
- Massachusetts Institute of Technology (US)
- Corresponding author
- Guarente, Leonard
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 1997-05
- Volume
- 89
- Issue
- 3
- Pages
- 381-391
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W1994369498
- Cited by
- 375
- References
- 59
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 6 · 2023: 9 · 2022: 4 · 2021: 8 · 2020: 3 · 2019: 10 · 2018: 11 · 2017: 7 · 2016: 12 · 2015: 11 · 2014: 10 · 2013: 17 · 2012: 11
- FWCI
- 11.50
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- IRIS (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion)
- Funders
- National Institute on Aging (AG11119)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Keywords
- Sir proteins, telomeric silencing, nucleolus, lifespan extension, aging, Sir3p, ribosomal DNA, Saccharomyces cerevisiae
- MeSH terms
- Cell Nucleolus, Fungal Proteins, Genes, Fungal, Molecular Sequence Data, Repressor Proteins, Saccharomyces cerevisiae, Trans-Activators, Gene Expression Regulation, Fungal, Mutagenesis, RNA-Binding Proteins, Telomere, Cellular Senescence, Sequence Homology, Amino Acid, Cell Cycle Proteins, Saccharomyces cerevisiae Proteins, Silent Information Regulator Proteins, Saccharomyces cerevisiae
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