Reducing sphingolipid synthesis orchestrates global changes to extend yeast lifespan.
Identifieur interne : 001015 ( Main/Corpus ); précédent : 001014; suivant : 001016Reducing sphingolipid synthesis orchestrates global changes to extend yeast lifespan.
Auteurs : Jun Liu ; Xinhe Huang ; Bradley R. Withers ; Eric Blalock ; Ke Liu ; Robert C. DicksonSource :
- Aging cell [ 1474-9726 ] ; 2013.
English descriptors
- KwdEn :
- MESH :
- chemical , biosynthesis : Sphingolipids.
- chemical , pharmacology : Antifungal Agents, Fatty Acids, Monounsaturated.
- drug effects : Yeasts.
- genetics : Yeasts.
- metabolism : Yeasts.
- physiology : Longevity.
- Animals, Gene Expression Regulation, Fungal, Signal Transduction.
Abstract
Studies of aging and longevity are revealing how diseases that shorten life can be controlled to improve the quality of life and lifespan itself. Two strategies under intense study to accomplish these goals are rapamycin treatment and calorie restriction. New strategies are being discovered including one that uses low-dose myriocin treatment. Myriocin inhibits the first enzyme in sphingolipid synthesis in all eukaryotes, and we showed recently that low-dose myriocin treatment increases yeast lifespan at least in part by down-regulating the sphingolipid-controlled Pkh1/2-Sch9 (ortholog of mammalian S6 kinase) signaling pathway. Here we show that myriocin treatment induces global effects and changes expression of approximately forty percent of the yeast genome with 1252 genes up-regulated and 1497 down-regulated (P < 0.05) compared with untreated cells. These changes are due to modulation of evolutionarily conserved signaling pathways including activation of the Snf1/AMPK pathway and down-regulation of the protein kinase A (PKA) and target of rapamycin complex 1 (TORC1) pathways. Many processes that enhance lifespan are regulated by these pathways in response to myriocin treatment including respiration, carbon metabolism, stress resistance, protein synthesis, and autophagy. These extensive effects of myriocin match those of rapamycin and calorie restriction. Our studies in yeast together with other studies in mammals reveal the potential of myriocin or related compounds to lower the incidence of age-related diseases in humans and improve health span.
DOI: 10.1111/acel.12107
PubMed: 23725375
PubMed Central: PMC3773046
Links to Exploration step
pubmed:23725375Le document en format XML
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Withers</name></author><author><name sortKey="Blalock, Eric" sort="Blalock, Eric" uniqKey="Blalock E" first="Eric" last="Blalock">Eric Blalock</name></author><author><name sortKey="Liu, Ke" sort="Liu, Ke" uniqKey="Liu K" first="Ke" last="Liu">Ke Liu</name></author><author><name sortKey="Dickson, Robert C" sort="Dickson, Robert C" uniqKey="Dickson R" first="Robert C" last="Dickson">Robert C. Dickson</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="RBID">pubmed:23725375</idno><idno type="pmid">23725375</idno><idno type="doi">10.1111/acel.12107</idno><idno type="pmc">PMC3773046</idno><idno type="wicri:Area/Main/Corpus">001015</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">001015</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Reducing sphingolipid synthesis orchestrates global changes to extend yeast lifespan.</title><author><name sortKey="Liu, Jun" sort="Liu, Jun" uniqKey="Liu J" first="Jun" last="Liu">Jun Liu</name><affiliation><nlm:affiliation>Key Laboratory of Bio-Resources and Eco-Environment of Ministry of Education, College of Life Science, Sichuan University, Chengdu, 610064, China; Department of Molecular and Cellular Biochemistry and the Lucille Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Huang, Xinhe" sort="Huang, Xinhe" uniqKey="Huang X" first="Xinhe" last="Huang">Xinhe Huang</name></author><author><name sortKey="Withers, Bradley R" sort="Withers, Bradley R" uniqKey="Withers B" first="Bradley R" last="Withers">Bradley R. Withers</name></author><author><name sortKey="Blalock, Eric" sort="Blalock, Eric" uniqKey="Blalock E" first="Eric" last="Blalock">Eric Blalock</name></author><author><name sortKey="Liu, Ke" sort="Liu, Ke" uniqKey="Liu K" first="Ke" last="Liu">Ke Liu</name></author><author><name sortKey="Dickson, Robert C" sort="Dickson, Robert C" uniqKey="Dickson R" first="Robert C" last="Dickson">Robert C. Dickson</name></author></analytic><series><title level="j">Aging cell</title><idno type="eISSN">1474-9726</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Antifungal Agents (pharmacology)</term><term>Fatty Acids, Monounsaturated (pharmacology)</term><term>Gene Expression Regulation, Fungal (MeSH)</term><term>Longevity (physiology)</term><term>Signal Transduction (MeSH)</term><term>Sphingolipids (biosynthesis)</term><term>Yeasts (drug effects)</term><term>Yeasts (genetics)</term><term>Yeasts (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Sphingolipids</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antifungal Agents</term><term>Fatty Acids, Monounsaturated</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Yeasts</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Yeasts</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Yeasts</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Longevity</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Gene Expression Regulation, Fungal</term><term>Signal Transduction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Studies of aging and longevity are revealing how diseases that shorten life can be controlled to improve the quality of life and lifespan itself. Two strategies under intense study to accomplish these goals are rapamycin treatment and calorie restriction. New strategies are being discovered including one that uses low-dose myriocin treatment. Myriocin inhibits the first enzyme in sphingolipid synthesis in all eukaryotes, and we showed recently that low-dose myriocin treatment increases yeast lifespan at least in part by down-regulating the sphingolipid-controlled Pkh1/2-Sch9 (ortholog of mammalian S6 kinase) signaling pathway. Here we show that myriocin treatment induces global effects and changes expression of approximately forty percent of the yeast genome with 1252 genes up-regulated and 1497 down-regulated (P < 0.05) compared with untreated cells. These changes are due to modulation of evolutionarily conserved signaling pathways including activation of the Snf1/AMPK pathway and down-regulation of the protein kinase A (PKA) and target of rapamycin complex 1 (TORC1) pathways. Many processes that enhance lifespan are regulated by these pathways in response to myriocin treatment including respiration, carbon metabolism, stress resistance, protein synthesis, and autophagy. These extensive effects of myriocin match those of rapamycin and calorie restriction. Our studies in yeast together with other studies in mammals reveal the potential of myriocin or related compounds to lower the incidence of age-related diseases in humans and improve health span. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23725375</PMID><DateCompleted><Year>2014</Year><Month>06</Month><Day>11</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1474-9726</ISSN><JournalIssue CitedMedium="Internet"><Volume>12</Volume><Issue>5</Issue><PubDate><Year>2013</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Aging cell</Title><ISOAbbreviation>Aging Cell</ISOAbbreviation></Journal><ArticleTitle>Reducing sphingolipid synthesis orchestrates global changes to extend yeast lifespan.</ArticleTitle><Pagination><MedlinePgn>833-41</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/acel.12107</ELocationID><Abstract><AbstractText>Studies of aging and longevity are revealing how diseases that shorten life can be controlled to improve the quality of life and lifespan itself. Two strategies under intense study to accomplish these goals are rapamycin treatment and calorie restriction. New strategies are being discovered including one that uses low-dose myriocin treatment. Myriocin inhibits the first enzyme in sphingolipid synthesis in all eukaryotes, and we showed recently that low-dose myriocin treatment increases yeast lifespan at least in part by down-regulating the sphingolipid-controlled Pkh1/2-Sch9 (ortholog of mammalian S6 kinase) signaling pathway. Here we show that myriocin treatment induces global effects and changes expression of approximately forty percent of the yeast genome with 1252 genes up-regulated and 1497 down-regulated (P < 0.05) compared with untreated cells. These changes are due to modulation of evolutionarily conserved signaling pathways including activation of the Snf1/AMPK pathway and down-regulation of the protein kinase A (PKA) and target of rapamycin complex 1 (TORC1) pathways. Many processes that enhance lifespan are regulated by these pathways in response to myriocin treatment including respiration, carbon metabolism, stress resistance, protein synthesis, and autophagy. These extensive effects of myriocin match those of rapamycin and calorie restriction. Our studies in yeast together with other studies in mammals reveal the potential of myriocin or related compounds to lower the incidence of age-related diseases in humans and improve health span. </AbstractText><CopyrightInformation>© 2013 The Anatomical Society and John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Jun</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Key Laboratory of Bio-Resources and Eco-Environment of Ministry of Education, College of Life Science, Sichuan University, Chengdu, 610064, China; Department of Molecular and Cellular Biochemistry and the Lucille Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Xinhe</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Withers</LastName><ForeName>Bradley R</ForeName><Initials>BR</Initials></Author><Author ValidYN="Y"><LastName>Blalock</LastName><ForeName>Eric</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Ke</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Dickson</LastName><ForeName>Robert C</ForeName><Initials>RC</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P20 GM103486</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AG024377</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AG024377</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P20GM103486</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal 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UI="C001996">thermozymocidin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000935" MajorTopicYN="N">Antifungal Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005229" MajorTopicYN="N">Fatty Acids, Monounsaturated</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015966" MajorTopicYN="N">Gene Expression Regulation, Fungal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008136" MajorTopicYN="N">Longevity</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013107" MajorTopicYN="N">Sphingolipids</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015003" MajorTopicYN="N">Yeasts</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">AMPK</Keyword><Keyword MajorTopicYN="N">S6 kinase</Keyword><Keyword MajorTopicYN="N">TORC1</Keyword><Keyword MajorTopicYN="N">aging</Keyword><Keyword MajorTopicYN="N">myriocin</Keyword><Keyword MajorTopicYN="N">sphingolipids</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="accepted"><Year>2013</Year><Month>05</Month><Day>25</Day></PubMedPubDate><PubMedPubDate 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