ArticleScientific reports2016
Crosstalk between cellular compartments protects against proteotoxicity and extends lifespan.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
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- Transgenic sensors reveal compartment-specific effects of aggregation-prone proteins on subcellular proteostasis during aging.Cell reports methods · 2024Article
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- The IRE1α pathway in glomerular diseases: The unfolded protein response and beyond.Frontiers in molecular medicine · 2022Review
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- 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
- Cross organelle stress response disruption promotes gentamicin-induced proteotoxicity.Cell death & disease · 2020Article
- Cell organelles and yeast longevity: an intertwined regulation.Current genetics · 2020Review
- Does Inter-Organellar Proteostasis Impact Yeast Quality and Performance During Beer Fermentation?Frontiers in genetics · 2020Article
- Mitochondria orchestrate proteostatic and metabolic stress responses.EMBO reports · 2019Review
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- Editorial: Mitochondrial Communication in Physiology, Disease and Aging.Frontiers in cell and developmental biology · 2019Article
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- pH homeostasis links the nutrient sensing PKA/TORC1/Sch9 ménage-à-trois to stress tolerance and longevity.Microbial cell (Graz, Austria) · 2018Review
- TORC1-mediated sensing of chaperone activity alters glucose metabolism and extends lifespan.Aging cell · 2017Article
- The heat shock response and humoral immune response are mutually antagonistic in honey bees.Scientific reports · 2017Article
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- Mechanisms Underlying the Essential Role of Mitochondrial Membrane Lipids in Yeast Chronological Aging.Oxidative medicine and cellular longevity · 2017Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In cells living under optimal conditions, protein folding defects are usually prevented by the action of chaperones. Here, we investigate the cell-wide consequences of loss of chaperone function in cytosol, mitochondria or the endoplasmic reticulum (ER) in budding yeast. We find that the decline in chaperone activity in each compartment results in loss of respiration, demonstrating the dependence of mitochondrial activity on cell-wide proteostasis. Furthermore, each chaperone deficiency triggers a response, presumably via the communication among the folding environments of distinct cellular compartments, termed here the cross-organelle stress response (CORE). The proposed CORE pathway encompasses activation of protein conformational maintenance machineries, antioxidant enzymes, and metabolic changes simultaneously in the cytosol, mitochondria, and the ER. CORE induction extends replicative and chronological lifespan in budding yeast, highlighting its protective role against moderate proteotoxicity and its consequences such as the decline in respiration. Our findings accentuate that organelles do not function in isolation, but are integrated in a functional crosstalk, while also highlighting the importance of organelle communication in aging and age-related diseases.
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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.