ArticlePLoS genetics2017
A Drosophila model for toxicogenomics: Genetic variation in susceptibility to heavy metal exposure.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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.
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.
Who cites it
39 citing papers in PubMed.
- The illusion of polygenicity in pool-seq genetic mapping studies: insufficient power can mask simple genetic architectures.Genetics · 2026Article
- Natural variation suggests candidate genes underlying Caenorhabditis elegans susceptibility to diverse toxicants.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- The Genetic Architecture of Venom Resistance: A Novel Approach to Target Identification and Coevolutionary Discovery.Molecular biology and evolution · 2026Article
- Artificial selection for resistance to copper and off-target physiological and behavioral effects in Drosophila melanogaster.Ecotoxicology and environmental safety · 2026Article
- Characterizing common loss-of-function genes and their potential utility in assessing population variability and chemical susceptibility.bioRxiv : the preprint server for biology · 2025Article
- Systems genetics of lifespan and senescence in Drosophila melanogaster.BMC biology · 2025Article
- Natural variation suggests candidate genes underlyingbioRxiv : the preprint server for biology · 2025Article
- Extreme QTL mapping enables the identification of novel zinc toxicity response loci in Drosophila melanogaster.Genetics · 2025Article
- Article
- Arsenic toxicity in theFrontiers in toxicology · 2025Article
- Drosophila Toxicogenomics: genetic variation and sexual dimorphism in susceptibility to 4-Methylimidazole.Human genomics · 2024Article
- Acute exposure to mercury drives changes in gene expression in Drosophila melanogaster.BMC research notes · 2024Article
- Gene expression variation underlying tissue-specific responses to copper stress in Drosophila melanogaster.G3 (Bethesda, Md.) · 2024Article
- Perspectives on the Drosophila melanogaster Model for Advances in Toxicological Science.Current protocols · 2023Review
- Gene expression variation underlying tissue-specific responses to copper stress inbioRxiv : the preprint server for biology · 2023Article
- Assessment of Chemical Toxicity in Adult Drosophila Melanogaster.Journal of visualized experiments : JoVE · 2023Article
- Fruit fly for anticancer drug discovery and repurposing.Annals of medicine and surgery (2012) · 2023Article
- Potentially toxic elements in the brains of people with multiple sclerosis.Scientific reports · 2023Article
- The toxic metal hypothesis for neurological disorders.Frontiers in neurology · 2023Article
- The genetic basis of adaptation to copper pollution inFrontiers in genetics · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
The genetic factors that give rise to variation in susceptibility to environmental toxins remain largely unexplored. Studies on genetic variation in susceptibility to environmental toxins are challenging in human populations, due to the variety of clinical symptoms and difficulty in determining which symptoms causally result from toxic exposure; uncontrolled environments, often with exposure to multiple toxicants; and difficulty in relating phenotypic effect size to toxic dose, especially when symptoms become manifest with a substantial time lag. Drosophila melanogaster is a powerful model that enables genome-wide studies for the identification of allelic variants that contribute to variation in susceptibility to environmental toxins, since the genetic background, environmental rearing conditions and toxic exposure can be precisely controlled. Here, we used extreme QTL mapping in an outbred population derived from the D. melanogaster Genetic Reference Panel to identify alleles associated with resistance to lead and/or cadmium, two ubiquitous environmental toxins that present serious health risks. We identified single nucleotide polymorphisms (SNPs) associated with variation in resistance to both heavy metals as well as SNPs associated with resistance specific to each of them. The effects of these SNPs were largely sex-specific. We applied mutational and RNAi analyses to 33 candidate genes and functionally validated 28 of them. We constructed networks of candidate genes as blueprints for orthologous networks of human genes. The latter not only provided functional contexts for known human targets of heavy metal toxicity, but also implicated novel candidate susceptibility genes. These studies validate Drosophila as a translational toxicogenomics gene discovery system.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.