PUBLICATION

Methyl mercury suppresses the formation of the tail primordium in developing zebrafish embryos

Authors
Yang, L., Ho, N.Y., Muller, F., and Strahle, U.
ID
ZDB-PUB-100302-11
Date
2010
Source
Toxicological sciences : an official journal of the Society of Toxicology   115(2): 379-390 (Journal)
Registered Authors
Ho, Nga Yu, Müller, Ferenc, Strähle, Uwe, Yang, Lixin
Keywords
zebrafish, methyl mercury, mmp9, mmp13, caudal fin primordium, fin fold, biosensor genes
MeSH Terms
  • Animals
  • Embryo, Nonmammalian/drug effects*
  • Embryo, Nonmammalian/embryology
  • Extremities/embryology
  • Gene Expression Regulation, Developmental/drug effects*
  • In Situ Hybridization
  • Matrix Metalloproteinase 13/genetics
  • Matrix Metalloproteinase 13/metabolism
  • Matrix Metalloproteinase 9/genetics
  • Matrix Metalloproteinase 9/metabolism
  • Methylmercury Compounds/toxicity*
  • Tail/drug effects
  • Tail/embryology
  • Water Pollutants, Chemical/toxicity*
  • Zebrafish/physiology*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
20181659 Full text @ Toxicol. Sci.
CTD
20181659
Abstract
The objective of this study was to characterize the mechanisms of action of the model environmental toxicant methyl mercury (MeHg) in the zebrafish embryo. Zebrafish embryos were exposed to MeHg and the effective concentration and window of exposure was determined in wildtype and fluorescent reporter transgenic zebrafish embryos. Genes were systematically assessed for altered expression in response to MeHg by in situ hybridization. MeHg impairs development of the fin fold and the tail fin primordium. Alterations in transgene expression were noted at 6 mug/l MeHg, making this shh:gfp line the most sensitive biosensor of MeHg exposure. The matrix metalloproteases mmp9 and mmp13 and 8 other genes are induced in the embryonic tail in response to MeHg. Our data suggest that MeHg impairs tail development at least partially by activation of the tissue remodelling proteases Mmp9 and Mmp13.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping