ArticleAlcoholism, clinical and experimental research2014
A screen of zebrafish mutants identifies ethanol-sensitive genetic loci.
Article in Alcoholism, clinical and experimental research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 71 citations in OpenAlex.
- Nicotine metabolites generate craniofacial defects that are worsened by ethanol exposure.PNAS nexus · 2026Article
- The Role of the Hedgehog Pathway in Alcohol-Induced Birth Defects.Advances in experimental medicine and biology · 2026Review
- Interactions between the bone morphogenetic protein and the planar cell polarity pathways lead to distinctive ethanol-induced facial defects.Alcohol, clinical & experimental research · 2025Article
- Mutations in the bone morphogenetic protein signaling pathway sensitize zebrafish and humans to ethanol-induced jaw malformations.Disease models & mechanisms · 2025Article
- Ethanol Induces Craniofacial Defects in Bmp Mutants Independent ofBiomedicines · 2025Article
- foxe1 mutant zebrafish show indications of a hypothyroid phenotype and increased sensitivity to ethanol for craniofacial malformations.Developmental dynamics : an official publication of the American Association of Anatomists · 2025Article
- Bone morphogenetic protein signaling pathway- Ethanol interactions disrupt palate formation independent of gata3.Reproductive toxicology (Elmsford, N.Y.) · 2025Article
- The Fetal Alcohol Spectrum Disorders-An Overview of Experimental Models, Therapeutic Strategies, and Future Research Directions.Children (Basel, Switzerland) · 2024Review
- Transforming growth factor beta signaling and craniofacial development: modeling human diseases in zebrafish.Frontiers in cell and developmental biology · 2024Review
- Alcohol exposure suppresses ribosome biogenesis and causes nucleolar stress in cranial neural crest cells.PloS one · 2024Article
- An Overview towards Zebrafish Larvae as a Model for Ocular Diseases.International journal of molecular sciences · 2023Review
- High-throughput detection of craniofacial defects in fluorescent zebrafish.Birth defects research · 2023Article
- Gene-alcohol interactions in birth defects.Current topics in developmental biology · 2023Article
- Loss ofFrontiers in neuroscience · 2023Article
- E-liquids and vanillin flavoring disrupts retinoic acid signaling and causes craniofacial defects in Xenopus embryos.Developmental biology · 2022Article
- Analysis of Gene-Environment Interactions Related to Developmental Disorders.Frontiers in pharmacology · 2022Review
- Zebrafish models of fetal alcohol spectrum disorders.Genesis (New York, N.Y. : 2000) · 2021Review
- Exposure to ethanol leads to midfacial hypoplasia in a zebrafish model of FASD via indirect interactions with the Shh pathway.BMC biology · 2021Article
- Multifactorial Genetic and Environmental Hedgehog Pathway Disruption Sensitizes Embryos to Alcohol-Induced Craniofacial Defects.Alcoholism, clinical and experimental research · 2020Article
- Animal models of gene-alcohol interactions.Birth defects research · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundFetal alcohol spectrum disorders (FASD) are a highly variable set of phenotypes caused by fetal alcohol exposure. Numerous factors influence FASD phenotypes, including genetics. The zebrafish is a powerful vertebrate model system with which to identify these genetic factors. Many zebrafish mutants are housed at the Zebrafish International Resource Center (ZIRC). These mutants are readily accessible and an excellent source to screen for ethanol (EtOH)-sensitive developmental structural mutants.
methodsWe screened mutants obtained from ZIRC for sensitivity to EtOH teratogenesis. Embryos were treated with 1% EtOH (41 mM tissue levels) from 6 hours postfertilization onward. Levels of apoptosis were evaluated at 24 hours postfertilization. At 4 days postfertilization, the craniofacial skeleton, peripheral axon projections, and sensory neurons of neuromasts were examined. Fish were genotyped to determine whether there were phenotype/genotype correlations.
resultsFive of 20 loci interacted with EtOH. Notable among these was that vangl2, involved in convergent extension movements of the embryonic axis, interacted strongly with EtOH. Untreated vangl2 mutants had normal craniofacial morphology, while severe midfacial defects including synophthalmia and narrowing of the palatal skeleton were found in all EtOH-treated mutants and a low percentage of heterozygotes. The cell cycle gene, plk1, also interacted strongly with EtOH. Untreated mutants have slightly elevated levels of apoptosis and loss of ventral craniofacial elements. Exposure to EtOH results in extensive apoptosis along with loss of neural tissue and the entire craniofacial skeleton. Phenotypes of hinfp, mars, and foxi1 mutants were also exacerbated by EtOH.
conclusionsOur results provide insight into the gene-EtOH interactions that may underlie EtOH teratogenesis. They support previous findings that EtOH disrupts elongation of the embryonic axis. Importantly, these results show that the zebrafish is an efficient model with which to test for gene-EtOH interactions. Understanding these interactions will be crucial to understanding of the FASD variation.
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.