ArticlePLoS genetics2014
Lifespan extension conferred by endoplasmic reticulum secretory pathway deficiency requires induction of the unfolded protein response.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 82 citations in OpenAlex.
- Organellar insights in ageing and longevity.Nature cell biology · 2026Review
- Article
- Thiolutin extends replicative lifespan by rewiring yeast transcription and metabolism.Scientific reports · 2026Article
- Role of Endoplasmic Reticulum Stress-Associated Genes in Septic Neonatal Foals.Antioxidants (Basel, Switzerland) · 2025Article
- Time-course transcriptome analysis reveals gene co-expression networks and transposable element responses to cold stress in cotton.BMC genomics · 2025Article
- Article
- CD44 correlates with longevity and enhances basal ATF6 activity and ER stress resistance.Cell reports · 2023Article
- The emergent role of mitochondrial surveillance in cellular health.Aging cell · 2022Review
- Multifarious Translational Regulation during Replicative Aging in Yeast.Journal of fungi (Basel, Switzerland) · 2022Article
- An Integrated Approach Reveals DNA Damage and Proteotoxic Stress as Main Effects of Proton Radiation inInternational journal of molecular sciences · 2022Article
- Article
- The Unfolded Protein Responses in Health, Aging, and Neurodegeneration: Recent Advances and Future Considerations.Frontiers in molecular neuroscience · 2022Review
- Reprogramming of the Ethanol Stress Response in Saccharomyces cerevisiae by the Transcription Factor Znf1 and Its Effect on the Biosynthesis of Glycerol and Ethanol.Applied and environmental microbiology · 2021Article
- Review
- Endoplasmic reticulum stress and glutathione therapeutics in chronic lung diseases.Redox biology · 2020Review
- Metformin attenuates the D‑galactose‑induced aging process via the UPR through the AMPK/ERK1/2 signaling pathways.International journal of molecular medicine · 2020Article
- Trajectories of Aging: How Systems Biology in Yeast Can Illuminate Mechanisms of Personalized Aging.Proteomics · 2020Review
- Article
- A functional unfolded protein response is required for chronological aging in Saccharomyces cerevisiae.Current genetics · 2020Article
- Cell organelles and yeast longevity: an intertwined regulation.Current genetics · 2020Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Cells respond to accumulation of misfolded proteins in the endoplasmic reticulum (ER) by activating the unfolded protein response (UPR) signaling pathway. The UPR restores ER homeostasis by degrading misfolded proteins, inhibiting translation, and increasing expression of chaperones that enhance ER protein folding capacity. Although ER stress and protein aggregation have been implicated in aging, the role of UPR signaling in regulating lifespan remains unknown. Here we show that deletion of several UPR target genes significantly increases replicative lifespan in yeast. This extended lifespan depends on a functional ER stress sensor protein, Ire1p, and is associated with constitutive activation of upstream UPR signaling. We applied ribosome profiling coupled with next generation sequencing to quantitatively examine translational changes associated with increased UPR activity and identified a set of stress response factors up-regulated in the long-lived mutants. Besides known UPR targets, we uncovered up-regulation of components of the cell wall and genes involved in cell wall biogenesis that confer resistance to multiple stresses. These findings demonstrate that the UPR is an important determinant of lifespan that governs ER stress and identify a signaling network that couples stress resistance to longevity.
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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.