Evidence map›Paper›PMID 29309688›Full record

ArticleMolecular biology and evolution2018

Genome-Wide Analysis of Starvation-Selected Drosophila melanogaster-A Genetic Model of Obesity.

Christopher M Hardy, Molly K Burke, Logan J Everett, Mira V Han, Kathryn M Lantz, Allen G Gibbs

Open access · bronzeAbstract read
In one paragraph

Article in Molecular biology and evolution, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

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  13. Natural alleles at theProceedings. Biological sciences · 2022
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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

6 authors at 3 institutions in 1 country.

Christopher M HardySchool of Life Sciences, University of Nevada Las Vegas, Las Vegas, NV.
Molly K BurkeDepartment of Integrative Biology, Oregon State University, Corvallis, OR.
Logan J EverettDepartment of Biological Sciences, North Carolina State University, Raleigh, NC.
Mira V HanSchool of Life Sciences, University of Nevada Las Vegas, Las Vegas, NV.
Kathryn M LantzSchool of Life Sciences, University of Nevada Las Vegas, Las Vegas, NV.
Allen G GibbsSchool of Life Sciences, University of Nevada Las Vegas, Las Vegas, NV.
University of Nevada, Las Vegas · USNorth Carolina State University · USOregon State University · US

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jared P Rutter · 1986 to 2026
$72.6M
Outreach/Diversity/Pipeline ProjectP20GM103440 · NIGMS · UNIVERSITY OF NEVADA RENO · PI Eduardo A Robleto · 2012 to 2026
$58.0M
Steroid Hormone Signaling in Genetically Obese DrosophilaR15GM100395 · NIGMS · UNIVERSITY OF NEVADA LAS VEGAS · PI ANDRES, ANDREW J, GIBBS, ALLEN · 2012 to 2012
$286k
NCI NIH HHS P30 CA042014NIGMS NIH HHS P20 GM103440NIGMS NIH HHS R15 GM100395
6 · The paper itself

Abstract

Experimental evolution affords the opportunity to investigate adaptation to stressful environments. Studies combining experimental evolution with whole-genome resequencing have provided insight into the dynamics of adaptation and a new tool to uncover genes associated with polygenic traits. Here, we selected for starvation resistance in populations of Drosophila melanogaster for over 80 generations. In response, the starvation-selected lines developed an obese condition, storing nearly twice the level of total lipids than their unselected controls. Although these fats provide a ∼3-fold increase in starvation resistance, the imbalance in lipid homeostasis incurs evolutionary cost. Some of these tradeoffs resemble obesity-associated pathologies in mammals including metabolic depression, low activity levels, dilated cardiomyopathy, and disrupted sleeping patterns. To determine the genetic basis of these traits, we resequenced genomic DNA from the selected lines and their controls. We found 1,046,373 polymorphic sites, many of which diverged between selection treatments. In addition, we found a wide range of genetic heterogeneity between the replicates of the selected lines, suggesting multiple mechanisms of adaptation. Genome-wide heterozygosity was low in the selected populations, with many large blocks of SNPs nearing fixation. We found candidate loci under selection by using an algorithm to control for the effects of genetic drift. These loci were mapped to a set of 382 genes, which associated with many processes including nutrient response, catabolic metabolism, and lipid droplet function. The results of our study speak to the evolutionary origins of obesity and provide new targets to understand the polygenic nature of obesity in a unique model system.

Indexed as

AcclimatizationAdaptation, PhysiologicalAnimalsDirected Molecular EvolutionDisease Models, AnimalDrosophila melanogasterEvolution, MolecularGenome, InsectGenome-Wide Association StudyModels, GeneticMultifactorial InheritanceObesitySelection, GeneticStarvationDrosophila melanogasterevolve and resequenceexperimental evolutionmetabolismobesitystarvation selection

Identifiers

PMID29309688
PMCPMC5850753
OpenAlexW2761207569

What OpenQuestion holds

Textmetadata
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.