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Article: Sir2 deletion prevents lifespan extension in 32 long-lived mutants
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TitleSir2 deletion prevents lifespan extension in 32 long-lived mutants
 
AuthorsDelaney, JR6
Sutphin, GL6
Dulken, B6
Sim, S6
Kim, JR6
Robison, B6 5
Schleit, J6
Murakami, CJ6
Carr, D6
An, EH6
Choi, E6
Chou, A6
Fletcher, M6
Jelic, M6
Liu, B4 3
Lockshon, D6 5
Moller, RM6
Pak, DN6
Peng, Q4 3
Peng, ZJ6
Pham, KM6
Sage, M6
Solanky, A6
Steffen, KK6
Tsuchiya, M6 5
Tsuchiyama, S6 5
Johnson, S6
Raabe, C6
Suh, Y1 3
Zhou, Z2
Liu, X4 3
Kennedy, BK6 5 3
Kaeberlein, M6 3
 
Issue Date2011
 
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/ACE
 
CitationAging Cell, 2011, v. 10 n. 6, p. 1089-1091 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1474-9726.2011.00742.x
 
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.
 
ISSN1474-9718
2013 Impact Factor: 5.939
 
DOIhttp://dx.doi.org/10.1111/j.1474-9726.2011.00742.x
 
ISI Accession Number IDWOS:000297003800018
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.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorDelaney, JR
 
dc.contributor.authorSutphin, GL
 
dc.contributor.authorDulken, B
 
dc.contributor.authorSim, S
 
dc.contributor.authorKim, JR
 
dc.contributor.authorRobison, B
 
dc.contributor.authorSchleit, J
 
dc.contributor.authorMurakami, CJ
 
dc.contributor.authorCarr, D
 
dc.contributor.authorAn, EH
 
dc.contributor.authorChoi, E
 
dc.contributor.authorChou, A
 
dc.contributor.authorFletcher, M
 
dc.contributor.authorJelic, M
 
dc.contributor.authorLiu, B
 
dc.contributor.authorLockshon, D
 
dc.contributor.authorMoller, RM
 
dc.contributor.authorPak, DN
 
dc.contributor.authorPeng, Q
 
dc.contributor.authorPeng, ZJ
 
dc.contributor.authorPham, KM
 
dc.contributor.authorSage, M
 
dc.contributor.authorSolanky, A
 
dc.contributor.authorSteffen, KK
 
dc.contributor.authorTsuchiya, M
 
dc.contributor.authorTsuchiyama, S
 
dc.contributor.authorJohnson, S
 
dc.contributor.authorRaabe, C
 
dc.contributor.authorSuh, Y
 
dc.contributor.authorZhou, Z
 
dc.contributor.authorLiu, X
 
dc.contributor.authorKennedy, BK
 
dc.contributor.authorKaeberlein, M
 
dc.date.accessioned2012-05-29T06:05:14Z
 
dc.date.available2012-05-29T06:05:14Z
 
dc.date.issued2011
 
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.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationAging Cell, 2011, v. 10 n. 6, p. 1089-1091 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1474-9726.2011.00742.x
 
dc.identifier.citeulike9760650
 
dc.identifier.doihttp://dx.doi.org/10.1111/j.1474-9726.2011.00742.x
 
dc.identifier.epage1091
 
dc.identifier.isiWOS:000297003800018
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.

 
dc.identifier.issn1474-9718
2013 Impact Factor: 5.939
 
dc.identifier.issue6
 
dc.identifier.pmid21902802
 
dc.identifier.scopuseid_2-s2.0-81155155530
 
dc.identifier.spage1089
 
dc.identifier.urihttp://hdl.handle.net/10722/147650
 
dc.identifier.volume10
 
dc.languageeng
 
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/ACE
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofAging Cell
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshDna-Binding Proteins - Deficiency - Genetics
 
dc.subject.meshGene Deletion
 
dc.subject.meshGene Expression Regulation, Fungal
 
dc.subject.meshGenotype
 
dc.subject.meshLongevity - Genetics
 
dc.subject.meshModels, Biological
 
dc.subject.meshObserver Variation
 
dc.subject.meshPhenotype
 
dc.subject.meshSaccharomyces Cerevisiae - Genetics - Metabolism
 
dc.subject.meshSaccharomyces Cerevisiae Proteins - Genetics
 
dc.subject.meshSilent Information Regulator Proteins, Saccharomyces Cerevisiae - Deficiency - Genetics
 
dc.subject.meshSirtuin 2 - Deficiency - Genetics
 
dc.titleSir2 deletion prevents lifespan extension in 32 long-lived mutants
 
dc.typeArticle
 
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Author Affiliations
  1. Albert Einstein College of Medicine of Yeshiva University
  2. The University of Hong Kong
  3. Guangdong Medical College
  4. Key Laboratory for Medical Molecular Diagnostics of Guangdong Province
  5. Buck Institute for Age Research
  6. University of Washington Seattle