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Article: Sir2 deletion prevents lifespan extension in 32 long-lived mutants

TitleSir2 deletion prevents lifespan extension in 32 long-lived mutants
Authors
Issue Date2011
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/ACE
Citation
Aging Cell, 2011, v. 10 n. 6, p. 1089-1091 How to Cite?
Abstract
Activation of Sir2 orthologs is proposed to increase lifespan downstream of dietary restriction. Here, we describe an examination of the effect of 32 different lifespan-extending mutations and four methods of DR on replicative lifespan (RLS) in the short-lived sir2Δ yeast strain. In every case, deletion of SIR2 prevented RLS extension; however, RLS extension was restored when both SIR2 and FOB1 were deleted in several cases, demonstrating that SIR2 is not directly required for RLS extension. These findings indicate that suppression of the sir2Δ lifespan defect is a rare phenotype among longevity interventions and suggest that sir2Δ cells senesce rapidly by a mechanism distinct from that of wild-type cells. They also demonstrate that failure to observe lifespan extension in a short-lived background, such as cells or animals lacking sirtuins, should be interpreted with caution. © 2011 The Authors. Aging Cell © 2011 Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland.
Persistent Identifierhttp://hdl.handle.net/10722/147650
ISSN
2013 Impact Factor: 5.939
ISI Accession Number ID
Funding AgencyGrant Number
NIHR01AG025549
T32AG000057
T32ES007032
National Natural Science Foundation of China30672205
30871440
30900739
30971620
31101051
Natural Science Foundation of Guangdong Province7301506
8452402301001450
9252402301000002
Key Foundation of Natural Science Research for Guangdong Universities06Z015
Funding Information:

This work was supported by NIH Grant R01AG025549. JRD, GLS and SJ were supported by NIH Training Grant T32AG000057. JS was supported by NIH Training Grant T32ES007032. XL is supported by The National Natural Science Foundation of China (30672205, 30871440, 30900739, 30971620, 31101051), The Natural Science Foundation of Guangdong Province (7301506, 8452402301001450, 9252402301000002) and Key Foundation of Natural Science Research for Guangdong Universities (06Z015). MK is an Ellison Medical Foundation New Scholar in Aging.

References

 

DC FieldValueLanguage
dc.contributor.authorDelaney, JRen_US
dc.contributor.authorSutphin, GLen_US
dc.contributor.authorDulken, Ben_US
dc.contributor.authorSim, Sen_US
dc.contributor.authorKim, JRen_US
dc.contributor.authorRobison, Ben_US
dc.contributor.authorSchleit, Jen_US
dc.contributor.authorMurakami, CJen_US
dc.contributor.authorCarr, Den_US
dc.contributor.authorAn, EHen_US
dc.contributor.authorChoi, Een_US
dc.contributor.authorChou, Aen_US
dc.contributor.authorFletcher, Men_US
dc.contributor.authorJelic, Men_US
dc.contributor.authorLiu, Ben_US
dc.contributor.authorLockshon, Den_US
dc.contributor.authorMoller, RMen_US
dc.contributor.authorPak, DNen_US
dc.contributor.authorPeng, Qen_US
dc.contributor.authorPeng, ZJen_US
dc.contributor.authorPham, KMen_US
dc.contributor.authorSage, Men_US
dc.contributor.authorSolanky, Aen_US
dc.contributor.authorSteffen, KKen_US
dc.contributor.authorTsuchiya, Men_US
dc.contributor.authorTsuchiyama, Sen_US
dc.contributor.authorJohnson, Sen_US
dc.contributor.authorRaabe, Cen_US
dc.contributor.authorSuh, Yen_US
dc.contributor.authorZhou, Zen_US
dc.contributor.authorLiu, Xen_US
dc.contributor.authorKennedy, BKen_US
dc.contributor.authorKaeberlein, Men_US
dc.date.accessioned2012-05-29T06:05:14Z-
dc.date.available2012-05-29T06:05:14Z-
dc.date.issued2011en_US
dc.identifier.citationAging Cell, 2011, v. 10 n. 6, p. 1089-1091en_US
dc.identifier.issn1474-9718en_US
dc.identifier.urihttp://hdl.handle.net/10722/147650-
dc.description.abstractActivation of Sir2 orthologs is proposed to increase lifespan downstream of dietary restriction. Here, we describe an examination of the effect of 32 different lifespan-extending mutations and four methods of DR on replicative lifespan (RLS) in the short-lived sir2Δ yeast strain. In every case, deletion of SIR2 prevented RLS extension; however, RLS extension was restored when both SIR2 and FOB1 were deleted in several cases, demonstrating that SIR2 is not directly required for RLS extension. These findings indicate that suppression of the sir2Δ lifespan defect is a rare phenotype among longevity interventions and suggest that sir2Δ cells senesce rapidly by a mechanism distinct from that of wild-type cells. They also demonstrate that failure to observe lifespan extension in a short-lived background, such as cells or animals lacking sirtuins, should be interpreted with caution. © 2011 The Authors. Aging Cell © 2011 Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/ACEen_US
dc.relation.ispartofAging Cellen_US
dc.subject.meshDna-Binding Proteins - Deficiency - Geneticsen_US
dc.subject.meshGene Deletionen_US
dc.subject.meshGene Expression Regulation, Fungalen_US
dc.subject.meshGenotypeen_US
dc.subject.meshLongevity - Geneticsen_US
dc.subject.meshModels, Biologicalen_US
dc.subject.meshObserver Variationen_US
dc.subject.meshPhenotypeen_US
dc.subject.meshSaccharomyces Cerevisiae - Genetics - Metabolismen_US
dc.subject.meshSaccharomyces Cerevisiae Proteins - Geneticsen_US
dc.subject.meshSilent Information Regulator Proteins, Saccharomyces Cerevisiae - Deficiency - Geneticsen_US
dc.subject.meshSirtuin 2 - Deficiency - Geneticsen_US
dc.titleSir2 deletion prevents lifespan extension in 32 long-lived mutantsen_US
dc.typeArticleen_US
dc.identifier.emailZhou, Z:zhongjun@hkucc.hku.hken_US
dc.identifier.authorityZhou, Z=rp00503en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1474-9726.2011.00742.xen_US
dc.identifier.pmid21902802en_US
dc.identifier.scopuseid_2-s2.0-81155155530en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-81155155530&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume10en_US
dc.identifier.issue6en_US
dc.identifier.spage1089en_US
dc.identifier.epage1091en_US
dc.identifier.isiWOS:000297003800018-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridDelaney, JR=37080385200en_US
dc.identifier.scopusauthoridSutphin, GL=23052900900en_US
dc.identifier.scopusauthoridDulken, B=52263404500en_US
dc.identifier.scopusauthoridSim, S=54417951800en_US
dc.identifier.scopusauthoridKim, JR=54417272200en_US
dc.identifier.scopusauthoridRobison, B=52264367300en_US
dc.identifier.scopusauthoridSchleit, J=36053659800en_US
dc.identifier.scopusauthoridMurakami, CJ=24076874200en_US
dc.identifier.scopusauthoridCarr, D=36834355000en_US
dc.identifier.scopusauthoridAn, EH=54416856700en_US
dc.identifier.scopusauthoridChoi, E=54417105000en_US
dc.identifier.scopusauthoridChou, A=54417114700en_US
dc.identifier.scopusauthoridFletcher, M=54417186400en_US
dc.identifier.scopusauthoridJelic, M=54417440600en_US
dc.identifier.scopusauthoridLiu, B=54417500300en_US
dc.identifier.scopusauthoridLockshon, D=6602733081en_US
dc.identifier.scopusauthoridMoller, RM=54417711200en_US
dc.identifier.scopusauthoridPak, DN=23992733500en_US
dc.identifier.scopusauthoridPeng, Q=44161318200en_US
dc.identifier.scopusauthoridPeng, ZJ=54417927600en_US
dc.identifier.scopusauthoridPham, KM=54417874000en_US
dc.identifier.scopusauthoridSage, M=54417783300en_US
dc.identifier.scopusauthoridSolanky, A=54418082200en_US
dc.identifier.scopusauthoridSteffen, KK=9336769600en_US
dc.identifier.scopusauthoridTsuchiya, M=12807375800en_US
dc.identifier.scopusauthoridTsuchiyama, S=52264568400en_US
dc.identifier.scopusauthoridJohnson, S=41861744300en_US
dc.identifier.scopusauthoridRaabe, C=54417848100en_US
dc.identifier.scopusauthoridSuh, Y=7202260379en_US
dc.identifier.scopusauthoridZhou, Z=8631856300en_US
dc.identifier.scopusauthoridLiu, X=47461459300en_US
dc.identifier.scopusauthoridKennedy, BK=26643504400en_US
dc.identifier.scopusauthoridKaeberlein, M=6602710772en_US
dc.identifier.citeulike9760650-

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