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      Evidence for the hallmarks of human aging in replicatively aging yeast

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      Author(s): 1 , 1 , *
      Publication date (Electronic, pub):
      Publication date (Electronic, collection):
      Journal: Microbial Cell
      Publisher: Shared Science Publishers OG
      Keywords: hallmarks of aging, human, replicative aging, yeast

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          Abstract

          Recently, efforts have been made to characterize the hallmarks that accompany and contribute to the phenomenon of aging, as most relevant for humans 1. Remarkably, studying the finite lifespan of the single cell eukaryote budding yeast (recently reviewed in 2 and 3) has been paramount for our understanding of aging. Here, we compile observations from literature over the past decades of research on replicatively aging yeast to highlight how the hallmarks of aging in humans are present in yeast. We find strong evidence for the majority of these, and summarize how yeast aging is especially characterized by the hallmarks of genomic instability, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, and mitochondrial dysfunction.

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          DNA methylation age of blood predicts all-cause mortality in later life

          Riccardo E Marioni, Sonia Shah, Allan McRae … (2015)
          Background DNA methylation levels change with age. Recent studies have identified biomarkers of chronological age based on DNA methylation levels. It is not yet known whether DNA methylation age captures aspects of biological age. Results Here we test whether differences between people’s chronological ages and estimated ages, DNA methylation age, predict all-cause mortality in later life. The difference between DNA methylation age and chronological age (Δage) was calculated in four longitudinal cohorts of older people. Meta-analysis of proportional hazards models from the four cohorts was used to determine the association between Δage and mortality. A 5-year higher Δage is associated with a 21% higher mortality risk, adjusting for age and sex. After further adjustments for childhood IQ, education, social class, hypertension, diabetes, cardiovascular disease, and APOE e4 status, there is a 16% increased mortality risk for those with a 5-year higher Δage. A pedigree-based heritability analysis of Δage was conducted in a separate cohort. The heritability of Δage was 0.43. Conclusions DNA methylation-derived measures of accelerated aging are heritable traits that predict mortality independently of health status, lifestyle factors, and known genetic factors. Electronic supplementary material The online version of this article (doi:10.1186/s13059-015-0584-6) contains supplementary material, which is available to authorized users.
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            Regulation of aging and age-related disease by DAF-16 and heat-shock factor.

            A.-L. Hsu (2003)
            The Caenorhabditis elegans transcription factor HSF-1, which regulates the heat-shock response, also influences aging. Reducing hsf-1 activity accelerates tissue aging and shortens life-span, and we show that hsf-1 overexpression extends lifespan. We find that HSF-1, like the transcription factor DAF-16, is required for daf-2-insulin/IGF-1 receptor mutations to extend life-span. Our findings suggest this is because HSF-1 and DAF-16 together activate expression of specific genes, including genes encoding small heat-shock proteins, which in turn promote longevity. The small heat-shock proteins also delay the onset of polyglutamine-expansion protein aggregation, suggesting that these proteins couple the normal aging process to this type of age-related disease.
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              Regulation of yeast replicative life span by TOR and Sch9 in response to nutrients.

              M Kaeberlein (2005)
              Calorie restriction increases life span in many organisms, including the budding yeast Saccharomyces cerevisiae. From a large-scale analysis of 564 single-gene-deletion strains of yeast, we identified 10 gene deletions that increase replicative life span. Six of these correspond to genes encoding components of the nutrient-responsive TOR and Sch9 pathways. Calorie restriction of tor1D or sch9D cells failed to further increase life span and, like calorie restriction, deletion of either SCH9 or TOR1 increased life span independent of the Sir2 histone deacetylase. We propose that the TOR and Sch9 kinases define a primary conduit through which excess nutrient intake limits longevity in yeast.
              Article 0 comments Cited 424 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Microb Cell
                Journal ID (iso-abbrev): Microb Cell
                Journal ID (pmc): Microb Cell
                Journal ID (publisher-id): Microb Cell
                Title: Microbial Cell
                Publisher: Shared Science Publishers OG
                ISSN (Electronic): 2311-2638
                Publication date (Electronic, pub): 20 June 2016
                Publication date (Electronic, collection): 04 July 2016
                Volume: 3
                Issue: 7
                Pages: 263-274
                Affiliations
                [1 ]European Research Institute for the Biology of Ageing, University of Groningen, University Medical Centre Groningen, Antonius Deusinglaan 1, 9713 AV, Groningen, The Netherlands.
                Author notes

                Conflict of interest: The authors declare no conflict of interest.

                Please cite this article as: Georges E. Janssens, Liesbeth M. Veenhoff (2016). Evidence for the hallmarks of human aging in replicatively aging yeast. Microbial Cell 3(7): 263-274. doi: 10.15698/mic2016.07.510

                Article
                Publisher ID: MIC0175E144
                DOI: 10.15698/mic2016.07.510
                PMC ID: 5354591
                PubMed ID: 28357364
                SO-VID: 849ff173-08fd-4551-96e9-be610a0cdd66
                Copyright statement: Copyright @ 2016
                License:

                This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.

                History
                Date received : 17 February 2016
                Date accepted : 20 April 2016
                Categories
                Subject: Microbiology
                Subject: Applied Microbiology
                Subject: Molecular Biology
                Subject: Genetics

                Keywords: hallmarks of aging,human,replicative aging,yeast
                Data availability:
                Keywords: hallmarks of aging, human, replicative aging, yeast

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