Evidence map›Paper›PMID 31747877›Full record

ArticleBMC bioinformatics2019

Estimating network changes from lifespan measurements using a parsimonious gene network model of cellular aging.

Hong Qin

Abstract read
In one paragraph

Article in BMC bioinformatics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

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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

1 author.

Hong QinDepartment of Computer Science and Engineering, Department of Biology, Geology and Environmental Science, SimCenter, University of Tennessee at Chattanooga, Chattanooga, 37403, TN, U.S.A.. qinstat@gmail.com.ORCID http://orcid.org/0000-0002-1060-6722

Funding

National Science Foundation 1453078National Science Foundation 1715985
6 · The paper itself

Abstract

backgroundCellular aging is best studied in the budding yeast Saccharomyces cerevisiae. As an example of a pleiotropic trait, yeast lifespan is influenced by hundreds of interconnected genes. However, no quantitative methods are currently available to infer system-level changes in gene networks during cellular aging.

resultsWe propose a parsimonious mathematical model of cellular aging based on stochastic gene interaction networks. This network model is made of only non-aging components: the strength of gene interactions declines with a constant mortality rate. Death of a cell occurs in the model when an essential node loses all of its interactions with other nodes, and is equivalent to the deletion of an essential gene. Stochasticity of gene interactions is modeled using a binomial distribution. We show that the exponential increase of mortality rate over time can emerge from this gene network model during the early stages of aging.We developed a maximal likelihood approach to estimate three lifespan-influencing network parameters from experimental lifespans: t

conclusionsOur theoretical model provides a parsimonious interpretation of experimental lifespan data from the perspective of gene networks. We hope that our work will stimulate more interest in developing network models to study aging as a pleiotropic trait.

Indexed as

Gene Regulatory NetworksModels, GeneticCellular SenescenceLikelihood FunctionsMutationPhenotypeReproducibility of ResultsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsStochastic ProcessesSaccharomyces cerevisiae ProteinsCellular agingGene networksGompertzReplicative lifespanSaccharomyces cerevisiae

Identifiers

PMID31747877
PMCPMC6865033

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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.