Evidence map›Paper›PMID 20421943›Full record

ArticlePLoS genetics2010

A microarray-based genetic screen for yeast chronological aging factors.

Mirela Matecic, Daniel L Smith, Xuewen Pan, Nazif Maqani, Stefan Bekiranov, Jef D Boeke, Jeffrey S Smith

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

123 citing papers in PubMed, 222 citations in OpenAlex.

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  10. Hypertrophic cardiomyopathy inThe journal of cardiovascular aging · 2024
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63 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 1 country.

Mirela MatecicDepartment of Biochemistry and Molecular Genetics, University of Virginia Health System, School of Medicine, Charlottesville, Virginia, United States of America.
Daniel L Smith
Xuewen Pan
Nazif Maqani
Stefan Bekiranov
Jef D Boeke
Jeffrey S Smith
University of Virginia · USUniversity of Virginia Health System · USHigh Throughput Biology (United States) · USJohns Hopkins University · US

Funding

Lesch-Nyhan Disease: A Model for Complex Genetic, Proteomic & Metabolic PathwaysR24DK082840 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FRIEDMANN, THEODORE · 2008 to 2012
$7.3M
NIA NIH HHS R01 AG022685NIDDK NIH HHS R24 DK082840
6 · The paper itself

Abstract

Model organisms have played an important role in the elucidation of multiple genes and cellular processes that regulate aging. In this study we utilized the budding yeast, Saccharomyces cerevisiae, in a large-scale screen for genes that function in the regulation of chronological lifespan, which is defined by the number of days that non-dividing cells remain viable. A pooled collection of viable haploid gene deletion mutants, each tagged with unique identifying DNA "bar-code" sequences was chronologically aged in liquid culture. Viable mutants in the aging population were selected at several time points and then detected using a microarray DNA hybridization technique that quantifies abundance of the barcode tags. Multiple short- and long-lived mutants were identified using this approach. Among the confirmed short-lived mutants were those defective for autophagy, indicating a key requirement for the recycling of cellular organelles in longevity. Defects in autophagy also prevented lifespan extension induced by limitation of amino acids in the growth media. Among the confirmed long-lived mutants were those defective in the highly conserved de novo purine biosynthesis pathway (the ADE genes), which ultimately produces IMP and AMP. Blocking this pathway extended lifespan to the same degree as calorie (glucose) restriction. A recently discovered cell-extrinsic mechanism of chronological aging involving acetic acid secretion and toxicity was suppressed in a long-lived ade4Delta mutant and exacerbated by a short-lived atg16Delta autophagy mutant. The identification of multiple novel effectors of yeast chronological lifespan will greatly aid in the elucidation of mechanisms that cells and organisms utilize in slowing down the aging process.

Indexed as

Oligonucleotide Array Sequence AnalysisCellular SenescenceGene Expression Regulation, FungalMutationSaccharomyces cerevisiae

Identifiers

PMID20421943
PMCPMC2858703
OpenAlexW2079783863

What OpenQuestion holds

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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.