Evidence map›Paper›PMID 20157595›Full record

ArticleAging2009

Extension of chronological life span by reduced TOR signaling requires down-regulation of Sch9p and involves increased mitochondrial OXPHOS complex density.

Yong Pan, Gerald S Shadel

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed
5.3field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

100 citing papers in PubMed, 153 citations in OpenAlex.

  1. Trial
  2. Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Metabolomic Profiling ofJournal of fungi (Basel, Switzerland) · 2026
    Article
  4. Review
  5. International journal of molecular sciences · 2023
    Review
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40 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Yong PanDepartment of Pathology, Yale University School of Medicine, New Haven CT 06520, USA.
Gerald S Shadel
Yale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The nutrient-sensing target of rapamycin (TOR) pathway appears to have a conserved role in regulating life span. This signaling network is complex, with many downstream physiological outputs, and thus the mechanisms underlying its age-related effects have not been elucidated fully. We demonstrated previously that reduced TOR signaling (intor1Delta strains) extends yeast chronological life span (CLS) by increasing mitochondrial oxygen consumption, in part, by up-regulating translation of mtDNA-encoded oxidative phosphorylation (OXPHOS) subunits. Here, we have examined in greater detail how TOR signaling influences mitochondrial function and CLS and the role of the Sch9p kinase in the TOR-mitochondria pathway. As is the case for oxygen consumption, mitochondrial translation is elevated in tor1Delta strains only during active growth and early stationary phase growth points. This is accompanied by a corresponding increase in the abundance of both mtDNA-encoded and nucleus-encoded OXPHOS subunits per mitochondrial mass. However, this increased OXPHOS complex density is not associated with more mitochondria/cell or cellular ATP and leads to an overall decrease in membrane potential, suggesting that TOR signaling may influence respiration uncoupling. Finally, we document that the Sch9p kinase is a key downstream effector of OXPHOS, ROS and CLS in the TOR-mitochondria pathway. Altogether, our results demonstrate that TOR signaling has a global role in regulating mitochondrial proteome dynamics and function that is important for its role in aging and provide compelling evidence for involvement of a "mitochondrial pre-conditioning" effect in CLS determination.

Indexed as

Cell ProliferationCell SurvivalDNA-Directed RNA PolymerasesDown-RegulationElectron Transport Chain Complex ProteinsElectron Transport Complex IVGene DeletionGene ExpressionLongevityMembrane Potential, MitochondrialMembrane ProteinsMitochondriaMitochondrial ProteinsOxidative PhosphorylationOxygen ConsumptionPhosphatidylinositol 3-KinasesDNA-Directed RNA PolymerasesElectron Transport Chain Complex ProteinsElectron Transport Complex IVMembrane ProteinsMitochondrial ProteinsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProtein Serine-Threonine KinasesReactive Oxygen SpeciesRibosomal ProteinsRPO41 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSCH9 protein, S cerevisiaeSirolimusTOR1 protein, S cerevisiaeVAR1 protein, S cerevisiaeaginglife spanmitochondriaproteomicsrespirationROSSCH9TOR1TOR signalingtranslation

Identifiers

PMID20157595
PMCPMC2815770
OpenAlexW15212789

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.