Danio rerio
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ABSTRACT:
PROVIDER: PRJNA105721 | ENA |
REPOSITORIES: ENA
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Project description:Exposure to environmental contaminants can disrupt normal development of the early vertebrate skeleton. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) impairs craniofacial skeletal development across many vertebrate species and its effects are especially prominent in early life stages of fish. TCDD activates the aryl hydrocarbon receptor (AHR), a transcription factor that mediates most if not all TCDD responses. We investigated the transcriptional response in the developing zebrafish jaw following TCDD exposure using DNA microarrays. Zebrafish larvae were exposed to TCDD at 96 h postfertilization (hpf) and jaw cartilage tissue was harvested for microarray analysis at 1, 2, 4 and 12 h postexposure (hpe). Numerous chondrogenic transcripts were misregulated by TCDD in the jaw. Comparison of transcripts altered by TCDD in jaw with transcripts altered in embryonic heart showed that the transcriptional responses in the jaw and the heart were strikingly different. Sox9b, a critical chondrogenic transcription factor, was the most significantly reduced transcript in the jaw. We hypothesized that the TCDD reduction of sox9b expression plays an integral role in affecting formation of the embryonic jaw. Morpholino knock down of sox9b expression demonstrated that partial reduction of sox9b expression alone was sufficient to produce a TCDD-like jaw phenotype. Heterozygous sox9b deletion mutant embryos were sensitized to TCDD. Lastly, embryos injected with sox9b mRNA and then exposed to TCDD blocked TCDD-induced jaw toxicity in approximately 14% of sox9b-injected embryos. These results suggest that reduced sox9b expression in TCDD-exposed zebrafish embryos contributes to jaw malformation. Keywords: Time course
2008-11-01 | GSE11893 | GEO
Project description:Exposure to environmental contaminants can disrupt normal development of the early vertebrate skeleton. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) impairs craniofacial skeletal development across many vertebrate species and its effects are especially prominent in early life stages of fish. TCDD activates the aryl hydrocarbon receptor (AHR), a transcription factor that mediates most if not all TCDD responses. We investigated the transcriptional response in the developing zebrafish jaw following TCDD exposure using DNA microarrays. Zebrafish larvae were exposed to TCDD at 96 h postfertilization (hpf) and jaw cartilage tissue was harvested for microarray analysis at 1, 2, 4 and 12 h postexposure (hpe). Numerous chondrogenic transcripts were misregulated by TCDD in the jaw. Comparison of transcripts altered by TCDD in jaw with transcripts altered in embryonic heart showed that the transcriptional responses in the jaw and the heart were strikingly different. Sox9b, a critical chondrogenic transcription factor, was the most significantly reduced transcript in the jaw. We hypothesized that the TCDD reduction of sox9b expression plays an integral role in affecting formation of the embryonic jaw. Morpholino knock down of sox9b expression demonstrated that partial reduction of sox9b expression alone was sufficient to produce a TCDD-like jaw phenotype. Heterozygous sox9b deletion mutant embryos were sensitized to TCDD. Lastly, embryos injected with sox9b mRNA and then exposed to TCDD blocked TCDD-induced jaw toxicity in approximately 14% of sox9b-injected embryos. These results suggest that reduced sox9b expression in TCDD-exposed zebrafish embryos contributes to jaw malformation. Experiment Overall Design: Three independent replicate microarray time course experiments were performed comparing transcript levels between TCDD-exposed and control zebrafish. For each experiment, zebrafish were exposed to TCDD for 1 h starting at 96 hpf as described above. For each time point (97, 98, 100 and 108 hpf) and treatment jaw samples were pooled from 10 dissections for RNA isolation and hybridization with Affymetrix zebrafish arrays (Affymetrix, Santa Clara, CA). Each microarray contains roughly 14,900 probes corresponding to approximately 30% of the zebrafish genome. For each array, total RNA (1 µg) was isolated from 10 jaw microdissections with the QIAGEN RNeasy Mini kit following the manufacturerâs protocol (QIAGEN, Valencia, CA). The One-Cycle Target Labeling and Control Reagents kit was used to synthesize cDNA and biotinylated cRNA following the manufacturerâs protocol (Affymetrix, Santa Clara, CA). Biotin-labeled cRNA (15 µg) was fragmented and hybridized onto Affymetrix Zebrafish Genechip Arrays following the protocol in the Affymetrix Genechip Expression Analysis Technical Manual. Following hybdrization, the arrays were washed and stained with streptavidin-phycoerythrin on an Affymetrix Fluidics Station 400 using the protocol EukGE WS2v4. Arrays were scanned with an Agilent Gene Array Scanner.
2008-11-13 | E-GEOD-11893 | biostudies-arrayexpress
Project description:MicroRNA expression profiling after short-term exposure to TCDD in zebrafish embryos [miRNA-Seq data]
| PRJNA171751 | ENA
Project description:AB* zebrafish embryos exposed to 1 ng/mL TCDD from 1d to 5d post-fertilization.
| PRJNA117085 | ENA
Project description:Transcriptomic analyses of TCDD treated zebrafish liver
| PRJNA215326 | ENA
Project description:MicroRNA expression profiling after short-term exposure to TCDD in zebrafish embryos [agilent and exiqon array data]
| PRJNA171750 | ENA
Project description:The aryl hydrocarbon receptor (AHR) repressor (AHRR), a bHLH-PAS protein, is a transcriptional repressor of AHR and other transcription factors (HIF, ER) and is regulated by an AHR-dependent mechanism. However, the physiological and toxicological roles of AHRR are not well understood. We demonstrated earlier that knockdown of AHRRa (one of two AHRR paralogs) in zebrafish embryos using morpholino anti-sense oligonucleotides results in developmental phenotypes such as pericardial edema, craniofacial malformations, and cardiac deformities, similar to effects caused by exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). AHRRa morphants also exhibit down-regulation of genes associated with photoreceptor development. To characterize the AHRRa function further, we used ZFN (zinc finger nuclease) technology to generate a line of zebrafish with a 7-bp deletion in exon 3 of AHRRa, leading to a truncated AHRR (110 aa, of which 38 are from AHRRa, compared to the 550-aa wild-type (wt) AHRRa). The mutant AHRRa protein, which contains basic regions but lacks the HLH and PAS domains, did not repress AHR in vitro, suggesting that it is inactive (null). Unlike AHRRa morphants, AHRRa-null fish did not display a TCDD-like phenotype; exposure to TCDD caused defects similar to those in TCDD-exposed wt embryos. RNA-sequencing revealed that basal expression of 562 genes differed significantly between the null and wt embryos, including down-regulation of genes associated with photoreceptor development, as seen in AHRRa morphants. TCDD-induced gene expression patterns for the prototypic AHR target genes were similar for null and wt embryos. However, 22 genes were differentially regulated by TCDD in the AHRRa-null embryos as compared to wt embryos (>2-fold; 5% FDR). We are currently investigating the link between these differentially expressed genes and the function of AHRRa in development and AHR signaling. [Supported by NIH R01ES006272]
2017-12-31 | GSE84420 | GEO
Project description:Altered basal and TCDD-induced gene expression in zebrafish embryos made AHRRa-null by ZFN-mediated gene targeting
| PRJNA329125 | ENA