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Nuclear tRNA sequestering slows aging by a mechanism similar to dietary restriction

ABSTRACT: Dietary restriction (DR) is the best-characterized intervention for slowing aging, and reduced signaling through the target of rapamycin (TOR) kinase is believed to be one of the key mechanisms by which DR extends life span in organisms from yeast to mammals. Here we describe a role for nuclear sequestration of tRNA in yeast replicative life span (RLS) extension from DR. DR causes the nuclear tRNA exporter Los1 to become depleted from the nucleus by a mechanism that requires the DNA damage response factor Rad53, and deletion of LOS1 or overexpression of RAD53 is sufficient to extend RLS. We further report that activation of the nitrogen responsive transcription factor Gln3 is the primary mechanism by which DR extends RLS. Gln3 is activated by both branches of the DR response and is required for life span extension. Overexpression of Gln3 extends RLS by approximately 50%.

ORGANISM(S): Saccharomyces cerevisiae Schizosaccharomyces pombe

PROVIDER: GSE37241 | GEO | 2015/02/03

SECONDARY ACCESSION(S): PRJNA159183

REPOSITORIES: GEO

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Nuclear tRNA sequestering slows aging by a mechanism similar to dietary restriction

Project description:Dietary restriction (DR) is the best-characterized intervention for slowing aging, and reduced signaling through the target of rapamycin (TOR) kinase is believed to be one of the key mechanisms by which DR extends life span in organisms from yeast to mammals. Here we describe a role for nuclear sequestration of tRNA in yeast replicative life span (RLS) extension from DR. DR causes the nuclear tRNA exporter Los1 to become depleted from the nucleus by a mechanism that requires the DNA damage response factor Rad53, and deletion of LOS1 or overexpression of RAD53 is sufficient to extend RLS. We further report that activation of the nitrogen responsive transcription factor Gln3 is the primary mechanism by which DR extends RLS. Gln3 is activated by both branches of the DR response and is required for life span extension. Overexpression of Gln3 extends RLS by approximately 50%. In order to identify potential factors acting to modulate longevity downstream of Los1, we used microarray analysis to compare the gene expression profiles of wild type and LOS1 knockout cells under non-restricted conditions cultured overnight prior to RNA isolation.

2015-02-03 | E-GEOD-37241 | biostudies-arrayexpress

Expression Data From Dietary Restriction, p53 Knockdown and sir2 Overexpression Mutants

Project description:Expression data from four different lifespan-extending conditions: dietary restriction in two different genetic backgrounds (canton-s and a yw, w1118 combination), sir2 overexpression and p53 knockdown (+/-). Comparison of significantly over and under-expressed genes reveals a signature for dietary restriction and lifespan extension. Abstract A major challenge in translating the positive effects of dietary restriction (DR) for the improvement of human health is the development of therapeutic mimics. One approach to finding DR mimics is based upon identification of the proximal effectors of DR life span extension. Whole genome profiling of DR in Drosophila shows a large number of changes in gene expression, making it difficult to establish which changes are involved in life span determination as opposed to other unrelated physiological changes. We used comparative whole genome expression profiling to discover genes whose change in expression is shared between DR and two molecular genetic life span extending interventions related to DR, increased dSir2 and decreased Dmp53 activity. We find twenty-one genes shared among the three related life span extending interventions. One of these genes, takeout, thought to be involved in circadian rhythms, feeding behavior and juvenile hormone binding is also increased in four other life span extending conditions: Rpd3, Indy, chico and methuselah. We demonstrate takeout is involved in longevity determination by specifically increasing adult takeout expression and extending life span. These studies demonstrate the power of comparative whole genome transcriptional profiling for identifying specific downstream elements of the DR life span extending pathway.

2011-01-20 | GSE26726 | GEO

Expression Data From Dietary Restriction, p53 Knockdown and sir2 Overexpression Mutants

2011-01-20 | E-GEOD-26726 | biostudies-arrayexpress

Significant and Systematic Expression Differentiation in Long-Lived Yeast Strains

Project description:The three yeast mutants sch9Δ, ras2Δ, tor1Δ show extended chronological life span up to three folds. This study aims to dissect the mechanisms that lead to the yeast life span extension. Keywords: Expression comparison between wild type and long-lived yeast mutant strain

2008-11-01 | GSE13420 | GEO

A role for SIR-2.1 regulation of ER stress response genes in determining C. elegans life span

Project description:This SuperSeries is composed of the following subset Series: GSE4093: Resveratrol treatment of daf-16 mutant C. elegans GSE4094: N2 worms treated with Resveratrol GSE4095: Sir-2.1 low copy transgenic Abstract: C. elegans SIR-2.1, a member of the Sir-2 family of NAD(+)-dependent protein deacetylases, has been shown to regulate nematode aging via the insulin/IGF pathway transcription factor daf-16. Treatment of C. elegans with the small molecule resveratrol, however, extends life span in a manner fully dependent upon sir-2.1, but independent of daf-16. Microarray analysis of worms treated with resveratrol demonstrates the transcriptional induction of a family of genes encoding prion-like glutamine/asparagine-rich proteins involved in endoplasmic reticulum (ER) stress response to unfolded proteins. RNA interference of abu-11, a member of this ER stress gene family, abolishes resveratrol-mediated life span extension, and overexpression of abu-11 extends the life span of transgenic animals. Furthermore, SIR-2.1 normally represses transcription of abu-11 and other ER stress gene family members, indicating that resveratrol extends life span by inhibiting sir-2.1-mediated repression of ER stress genes. Our findings demonstrate that abu-11 and other members of its ER stress gene family are positive determinants of C. elegans life span. Refer to individual Series

2006-03-07 | E-GEOD-4402 | biostudies-arrayexpress

The role of Sgf73 occupancy

Project description:Sgf73, a core component of the SAGA (Spt-Ada-Gcn5 Acetyltransferase) co-activator complex, is the yeast orthologue of ataxin-7, which in humans undergoes CAG ? polyglutamine repeat expansion to produce the neurodegenerative disease spinocerebellar ataxia type 7 (SCA7). We recently documented that deletion of SGF73 dramatically extends replicative lifespan (RLS) in yeast. To define the basis for Sgf73-mediated RLS extension, and to further explore the molecular function of Sgf73/ataxin-7 we performed ChIP-Seq for Sgf73 in yeast to identify its regions of DNA binding. The aim of the study was to uncover the underlying mechanisms controlled by Sgf73. This information will be used to understand the role of Sgf73 target genes in yeast aging pathways and possibly highlight pathways of mammalian aging regulation and SCA7 neurodegeneration in humans.

2017-06-12 | GSE76461 | GEO

A role for SIR-2.1 regulation of ER stress response genes in determining C. elegans life span

Project description:Abstract: C. elegans SIR-2.1, a member of the Sir-2 family of NAD(+)-dependent protein deacetylases, has been shown to regulate nematode aging via the insulin/IGF pathway transcription factor daf-16. Treatment of C. elegans with the small molecule resveratrol, however, extends life span in a manner fully dependent upon sir-2.1, but independent of daf-16. Microarray analysis of worms treated with resveratrol demonstrates the transcriptional induction of a family of genes encoding prion-like glutamine/asparagine-rich proteins involved in endoplasmic reticulum (ER) stress response to unfolded proteins. RNA interference of abu-11, a member of this ER stress gene family, abolishes resveratrol-mediated life span extension, and overexpression of abu-11 extends the life span of transgenic animals. Furthermore, SIR-2.1 normally represses transcription of abu-11 and other ER stress gene family members, indicating that resveratrol extends life span by inhibiting sir-2.1-mediated repression of ER stress genes. Our findings demonstrate that abu-11 and other members of its ER stress gene family are positive determinants of C. elegans life span. This SuperSeries is composed of the SubSeries listed below.

2006-03-08 | GSE4402 | GEO

Bre1-mediated Set2 protein degradation promotes chronological aging in budding yeast [RNA-seq]

Project description:Histone modification affects life span in various organisms. The loss of Histone H3K36 methylation can shorten replicative life span in Saccharomyces cerevisiae. However, budding yeast, as a model organism for aging research, has replicative life span (RLS) and chronological life span (CLS). In this study, we showed that the loss of Histone H3K36 methylation can shorten CLS in Saccharomyces cerevisiae. We identified Ubc3/Bre1 mediates polyubiquitination of Set2 K25 and K530 at log phase and stationary phase, and Bre1 interacts with Ubc3 and Rad6 simultaneously. BRE1 knockout can stabilize Set2 protein to maintain H3K36me3 and regulate the transcription of aging related genes, such as DSE1/DSE2/SUN4/EGT2/SCW11. We also proved that Gcn5-mediated Set2 acetylation regulates Set2 protein stability and chronological aging. Altogether, our study showed that knockout of BRE1 and GCN5 regulate Set2 protein level by mediating the polyubiquitination of Set2 to influence the level of H3K36me3 and the transcription level of aging related genes enriched by H3K36me3, thereby extending the chronological life span.

2023-09-29 | GSE221025 | GEO

Bre1-mediated Set2 protein degradation promotes chronological aging in budding yeast [ChIP-seq]

2023-09-29 | GSE221024 | GEO

Time-course gene expression profiles of a Saccharomyces cerevisiae wild type and long-lived sch9-delta mutant

Project description:The SCH9 null strain has smaller cell size, grows at a slower rate and survives three times longer than wide-type yeast. This study aims to dissect the mechanisms that lead to the yeast life span extension of sch9-delta.

2009-12-25 | GSE14227 | GEO

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