PUBLICATION
2,3,7,8-Tetrachlorodibenzo-p-dioxin Upregulates FoxQ1b in Zebrafish Jaw Primordium
- Authors
- Planchart, A., and Mattingly, C.J.
- ID
- ZDB-PUB-100112-23
- Date
- 2010
- Source
- Chemical Research in Toxicology 23(3): 480-487 (Journal)
- Registered Authors
- Keywords
- none
- MeSH Terms
-
- Animals
- Embryo, Nonmammalian/metabolism
- Enhancer Elements, Genetic
- Environmental Pollutants/pharmacology*
- Forkhead Transcription Factors/genetics*
- Gene Expression Regulation, Developmental/drug effects*
- Jaw/metabolism
- Jaw/pathology
- Jaw Abnormalities/chemically induced
- Receptors, Aryl Hydrocarbon/metabolism
- Up-Regulation/drug effects
- Zebrafish/genetics*
- Zebrafish/metabolism
- Zebrafish Proteins/genetics*
- Zebrafish Proteins/metabolism
- PubMed
- 20055451 Full text @ Chem. Res. Toxicol.
- CTD
- 20055451
Citation
Planchart, A., and Mattingly, C.J. (2010) 2,3,7,8-Tetrachlorodibenzo-p-dioxin Upregulates FoxQ1b in Zebrafish Jaw Primordium. Chemical Research in Toxicology. 23(3):480-487.
Abstract
Vertebrate jaw development can be disrupted by exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-a potent activator of the aryl hydrocarbon receptor (AHR) transcription factor required for transducing the toxic effects of TCDD. We used zebrafish (Danio rerio) embryos to investigate transcriptional responses to TCDD with the goal of discovering novel, jaw-specific genes affected by TCDD exposure. Our results uncovered a novel target of TCDD-activated Ahr belonging to the evolutionarily conserved family of forkhead box transcription factors. Quantitative real-time polymerase chain reaction analysis demonstrated that FoxQ1b was upregulated by TCDD 7- and 10-fold at 24 and 48 h postfertilization (hpf), respectively. The rate of TCDD-induced FoxQ1b expression was more rapid than that of Cyp1a, a known direct target of TCDD-activated Ahr. TCDD-mediated induction of FoxQ1b was suppressed in the presence of an Ahr antagonist, alpha-naphthoflavone, as well as following knockdown of Ahr2 expression using an Ahr2-specific morpholino antisense oligonucleotide. In situ hybridization analysis of FoxQ1b expression at 48 hpf demonstrated that FoxQ1b is specifically expressed in the jaw primordium where it discretely outlines a developing jaw structure known as Meckel's cartilage-a conserved structure in all jawed vertebrates that develops abnormally in the presence of TCDD. These results identify a novel target of TCDD-activated Ahr and suggest that FoxQ1b may play a role in craniofacial abnormalities induced by developmental exposure to TCDD.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping