The yeast replicative aging model.
Identifieur interne : 000443 ( Main/Exploration ); précédent : 000442; suivant : 000444The yeast replicative aging model.
Auteurs : Chong He [États-Unis] ; Chuankai Zhou [États-Unis] ; Brian K. Kennedy [Singapour]Source :
- Biochimica et biophysica acta. Molecular basis of disease [ 0925-4439 ] ; 2018.
Descripteurs français
- KwdFr :
- Chromatine (métabolisme), Division cellulaire (MeSH), Instabilité du génome (MeSH), Longévité (génétique), Modèles biologiques (MeSH), Protein-Serine-Threonine Kinases (génétique), Protein-Serine-Threonine Kinases (métabolisme), Protéines SIR de Saccharomyces cerevisiae (génétique), Protéines SIR de Saccharomyces cerevisiae (métabolisme), Protéines de Saccharomyces cerevisiae (génétique), Protéines de Saccharomyces cerevisiae (métabolisme), Réplication de l'ADN (MeSH), Saccharomyces cerevisiae (génétique), Sirtuine-2 (génétique), Sirtuine-2 (métabolisme), Transduction du signal (génétique), Transduction du signal (physiologie), Vieillissement (génétique), Vieillissement (physiologie).
- MESH :
- génétique : Longévité, Protein-Serine-Threonine Kinases, Protéines SIR de Saccharomyces cerevisiae, Protéines de Saccharomyces cerevisiae, Saccharomyces cerevisiae, Sirtuine-2, Transduction du signal, Vieillissement.
- métabolisme : Chromatine, Protein-Serine-Threonine Kinases, Protéines SIR de Saccharomyces cerevisiae, Protéines de Saccharomyces cerevisiae, Sirtuine-2.
- physiologie : Transduction du signal, Vieillissement.
- Division cellulaire, Instabilité du génome, Modèles biologiques, Réplication de l'ADN.
English descriptors
- KwdEn :
- Aging (genetics), Aging (physiology), Cell Division (MeSH), Chromatin (metabolism), DNA Replication (MeSH), Genomic Instability (MeSH), Longevity (genetics), Models, Biological (MeSH), Protein-Serine-Threonine Kinases (genetics), Protein-Serine-Threonine Kinases (metabolism), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (genetics), Signal Transduction (physiology), Silent Information Regulator Proteins, Saccharomyces cerevisiae (genetics), Silent Information Regulator Proteins, Saccharomyces cerevisiae (metabolism), Sirtuin 2 (genetics), Sirtuin 2 (metabolism).
- MESH :
- chemical , genetics : Protein-Serine-Threonine Kinases, Saccharomyces cerevisiae Proteins, Silent Information Regulator Proteins, Saccharomyces cerevisiae, Sirtuin 2.
- chemical , metabolism : Chromatin, Protein-Serine-Threonine Kinases, Saccharomyces cerevisiae Proteins, Silent Information Regulator Proteins, Saccharomyces cerevisiae, Sirtuin 2.
- genetics : Aging, Longevity, Saccharomyces cerevisiae, Signal Transduction.
- physiology : Aging, Signal Transduction.
- Cell Division, DNA Replication, Genomic Instability, Models, Biological.
Abstract
It has been nearly three decades since the budding yeast Saccharomyces cerevisiae became a significant model organism for aging research and it has emerged as both simple and powerful. The replicative aging assay, which interrogates the number of times a "mother" cell can divide and produce "daughters", has been a stalwart in these studies, and genetic approaches have led to the identification of hundreds of genes impacting lifespan. More recently, cell biological and biochemical approaches have been developed to determine how cellular processes become altered with age. Together, the tools are in place to develop a holistic view of aging in this single-celled organism. Here, we summarize the current state of understanding of yeast replicative aging with a focus on the recent studies that shed new light on how aging pathways interact to modulate lifespan in yeast.
DOI: 10.1016/j.bbadis.2018.02.023
PubMed: 29524633
Affiliations:
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The replicative aging assay, which interrogates the number of times a "mother" cell can divide and produce "daughters", has been a stalwart in these studies, and genetic approaches have led to the identification of hundreds of genes impacting lifespan. More recently, cell biological and biochemical approaches have been developed to determine how cellular processes become altered with age. Together, the tools are in place to develop a holistic view of aging in this single-celled organism. Here, we summarize the current state of understanding of yeast replicative aging with a focus on the recent studies that shed new light on how aging pathways interact to modulate lifespan in yeast.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29524633</PMID><DateCompleted><Year>2018</Year><Month>11</Month><Day>26</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0925-4439</ISSN><JournalIssue CitedMedium="Print"><Volume>1864</Volume><Issue>9 Pt A</Issue><PubDate><Year>2018</Year><Month>09</Month></PubDate></JournalIssue><Title>Biochimica et biophysica acta. Molecular basis of disease</Title><ISOAbbreviation>Biochim Biophys Acta Mol Basis Dis</ISOAbbreviation></Journal><ArticleTitle>The yeast replicative aging model.</ArticleTitle><Pagination><MedlinePgn>2690-2696</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0925-4439(18)30080-2</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbadis.2018.02.023</ELocationID><Abstract><AbstractText>It has been nearly three decades since the budding yeast Saccharomyces cerevisiae became a significant model organism for aging research and it has emerged as both simple and powerful. The replicative aging assay, which interrogates the number of times a "mother" cell can divide and produce "daughters", has been a stalwart in these studies, and genetic approaches have led to the identification of hundreds of genes impacting lifespan. More recently, cell biological and biochemical approaches have been developed to determine how cellular processes become altered with age. Together, the tools are in place to develop a holistic view of aging in this single-celled organism. Here, we summarize the current state of understanding of yeast replicative aging with a focus on the recent studies that shed new light on how aging pathways interact to modulate lifespan in yeast.</AbstractText><CopyrightInformation>Copyright © 2018. Published by Elsevier B.V.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>He</LastName><ForeName>Chong</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Buck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA 94945, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Chuankai</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Buck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA 94945, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kennedy</LastName><ForeName>Brian K</ForeName><Initials>BK</Initials><AffiliationInfo><Affiliation>Buck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA 94945, USA; Departments of Biochemistry and Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore. 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MajorTopicYN="N">Sirtuin 2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Cell asymmetry</Keyword><Keyword MajorTopicYN="Y">Dietary restriction (DR)</Keyword><Keyword MajorTopicYN="Y">Mitochondria</Keyword><Keyword MajorTopicYN="Y">Proteostasis</Keyword><Keyword MajorTopicYN="Y">Reactive oxygen species (ROS)</Keyword><Keyword MajorTopicYN="Y">Replicative lifespan (RLS)</Keyword><Keyword MajorTopicYN="Y">Retrograde response</Keyword><Keyword MajorTopicYN="Y">Ribosomal DNA (rDNA)</Keyword><Keyword MajorTopicYN="Y">Sirtuins</Keyword><Keyword MajorTopicYN="Y">Target of rapamycin (TOR)</Keyword><Keyword MajorTopicYN="Y">Ubiquitin/proteasome system (UPS)</Keyword><Keyword MajorTopicYN="Y">Yeast aging</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate 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