Evidence map›Paper›PMID 25329157›Full record

ArticlePLoS computational biology2014

Likelihood-based gene annotations for gap filling and quality assessment in genome-scale metabolic models.

Matthew N Benedict, Michael B Mundy, Christopher S Henry, Nicholas Chia, Nathan D Price

Abstract read
In one paragraph

Article in PLoS computational biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing 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

43 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

5 authors.

Matthew N BenedictDepartment of Chemical and Biomolecular Engineering, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.
Michael B MundyCenter for Individualized Medicine, Mayo Clinic, Rochester, Minnesota, United States of America.
Christopher S HenryMathematics and Computer Science Division, Argonne National Laboratory, Lemont, Illinois, United States of America.
Nicholas ChiaCenter for Individualized Medicine, Mayo Clinic, Rochester, Minnesota, United States of America; Department of Surgery, Mayo Clinic, Rochester, Minnesota, United States of America; Department of Physiology and Bioengineering, Mayo Clinic, Rochester, Minnesota, United States of America.
Nathan D PriceDepartment of Chemical and Biomolecular Engineering, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America; Institute for Systems Biology, Seattle, Washington, United States of America.

Funding

Microbial Metabolic Toxicity Drives Colon CancerR01CA179243 · NCI · MAYO CLINIC ROCHESTER · PI CHIA, NICHOLAS · 2014 to 2018
$2.0M
NCI NIH HHS R01 CA179243
6 · The paper itself

Abstract

Genome-scale metabolic models provide a powerful means to harness information from genomes to deepen biological insights. With exponentially increasing sequencing capacity, there is an enormous need for automated reconstruction techniques that can provide more accurate models in a short time frame. Current methods for automated metabolic network reconstruction rely on gene and reaction annotations to build draft metabolic networks and algorithms to fill gaps in these networks. However, automated reconstruction is hampered by database inconsistencies, incorrect annotations, and gap filling largely without considering genomic information. Here we develop an approach for applying genomic information to predict alternative functions for genes and estimate their likelihoods from sequence homology. We show that computed likelihood values were significantly higher for annotations found in manually curated metabolic networks than those that were not. We then apply these alternative functional predictions to estimate reaction likelihoods, which are used in a new gap filling approach called likelihood-based gap filling to predict more genomically consistent solutions. To validate the likelihood-based gap filling approach, we applied it to models where essential pathways were removed, finding that likelihood-based gap filling identified more biologically relevant solutions than parsimony-based gap filling approaches. We also demonstrate that models gap filled using likelihood-based gap filling provide greater coverage and genomic consistency with metabolic gene functions compared to parsimony-based approaches. Interestingly, despite these findings, we found that likelihoods did not significantly affect consistency of gap filled models with Biolog and knockout lethality data. This indicates that the phenotype data alone cannot necessarily be used to discriminate between alternative solutions for gap filling and therefore, that the use of other information is necessary to obtain a more accurate network. All described workflows are implemented as part of the DOE Systems Biology Knowledgebase (KBase) and are publicly available via API or command-line web interface.

Indexed as

Models, GeneticAlgorithmsGenomicsMetabolomicsModels, StatisticalMolecular Sequence AnnotationPhenotypeSensitivity and Specificity

Identifiers

PMID25329157
PMCPMC4199484

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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.