ArticleToxicology in vitro : an international journal published in association with BIBRA2012
The effects of methylmercury on Notch signaling during embryonic neural development in Drosophila melanogaster.
Article in Toxicology in vitro : an international journal published in association with BIBRA, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed.
- Review: myogenic and muscle toxicity targets of environmental methylmercury exposure.Archives of toxicology · 2024Review
- Notch Signaling in Insect Development: A Simple Pathway with Diverse Functions.International journal of molecular sciences · 2023Review
- Disease-associated metabolic pathways affected by heavy metals and metalloid.Toxicology reports · 2023Review
- Post-Developmental Roles of Notch Signaling in the Nervous System.Biomolecules · 2020Review
- Guarana improves behavior and inflammatory alterations triggered by methylmercury exposure: an in vivo fruit fly and in vitro neural cells study.Environmental science and pollution research international · 2019Article
- Drosophotoxicology: Elucidating Kinetic and Dynamic Pathways of Methylmercury Toxicity in a Drosophila Model.Frontiers in genetics · 2019Article
- The road less traveled: from genotype to phenotype in flies and humans.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Article
- Methylmercury exposure causes a persistent inhibition of myogenin expression and C2C12 myoblast differentiation.Toxicology · 2018Article
- Notch Target Gene E(spl)mδ Is a Mediator of Methylmercury-Induced Myotoxicity inFrontiers in genetics · 2017Article
- A method of permeabilization of Drosophila embryos for assays of small molecule activity.Journal of visualized experiments : JoVE · 2014Article
- Article
- Developmental study of mercury effects on the fruit fly (Drosophila melanogaster).Interdisciplinary toxicology · 2013Article
- Methylmercury exposure during early Xenopus laevis development affects cell proliferation and death but not neural progenitor specification.Neurotoxicology and teratologyArticle
- The Notch target E(spl)mδ is a muscle-specific gene involved in methylmercury toxicity in motor neuron development.Neurotoxicology and teratologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Methylmercury (MeHg) is a ubiquitous toxicant that targets the developing fetal nervous system. MeHg interacts with the Notch signaling pathway, a highly-conserved intercellular signaling mechanism required for normal development. Notch signaling is conveyed by activation of the genes in the enhancer of split (E(spl)) locus in Drosophila. We have previously shown that acute high doses of MeHg upregulate several E(spl) genes in Drosophila neural-derived C6 cells. Furthermore, MeHg induction of E(spl) can occur independent of the Notch receptor itself. We now show that MeHg, unlike inorganic mercury (HgCl2), preferentially upregulates E(spl)mδ and E(spl)mγ in Drosophila C6 cells. This is distinct from Delta ligand-induced Notch signaling in which no induction of E(spl)mδ is seen. MeHg is also seen to specifically upregulate E(spl)mδ in Drosophila embryos where HgCl2 showed no such effect. Additionally, treatment of embryos with MeHg caused a consistent failure in axonal outgrowth of the intersegmental nerve (ISN). This ISN phenotype was partially replicated by genetic activation of the Notch pathway, but was not replicated by increasing expression of E(spl)mδ. These data suggest a role for Notch signaling and the E(spl)mδ target gene in MeHg toxicity, however, the site of action for E(spl)mδ in this system remains to be elucidated.
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.