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Aryl hydrocarbon receptor mediates larval zebrafish fin duplication following exposure to benzofluoranthenes.

ABSTRACT: Aryl hydrocarbon receptor mediates larval zebrafish fin duplication following exposure to benzofluoranthenes.

PROVIDER: PRJNA602305 | ENA |

REPOSITORIES: ENA

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Aryl hydrocarbon receptor mediates larval zebrafish fin duplication following exposure to benzofluoranthenes.

Project description:Polycyclic aromatic hydrocarbons (PAHs) can alter gene expression by acting through the aryl hydrocarbon receptor (AHR). In a previous phenotypic screen of over 120 PAHs, we identified four PAHs that induce an ectopic caudal fin (called X-fin) in larval zebrafish: benzo[k]fluoranthene (BkF), dibenzo[b,k]fluoranthene, dibenzo[a,h]anthracene, and benzo[j]fluoranthene. We investigated several plausible mechanisms of X-fin formation using the most potent X-fin inducer, BkF. The X-fin phenotype was dependent on the AHR paralog Ahr2, and we performed RNA sequencing to identify altered gene expression patterns. Transcriptional profiles of distal trunk tissue, where the phenotype was manifest, were generated for animals exposed to 1% DMSO (control) or 12 μM BkF. Four time points of X-fin development were considered for transcriptomics: prior to visual emergence of X-fin (48 hpf), during manifestation of disrupted caudal fin fold development (60 and 72 hpf), and after emergence of X-fin (96 hpf).

2020-01-21 | GSE143945 | GEO

Aryl Hydrocarbon Receptor Mediates Larval Zebrafish Fin Duplication Following Exposure to Benzofluoranthenes.

Project description: Not available

| S-EPMC7357178 | biostudies-literature

Transcription profiling of zebrafish larval regenerating fin tissue after exposure to TCDD in order to identify genes differentially regulated after Ahr activation

Project description:Exposures to dioxin, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) cause a wide array of toxicities in vertebrates and is mostly considered to be mediated through the inappropriate activation of the aryl hydrocarbon receptor (Ahr) signaling pathway. Although transcriptional regulation by Ahr is widely studied, the molecular mechanisms responsible for the adverse outcomes after Ahr activation are largely unknown. To identify the important events downstream of AHR activation that play an actual role in the toxic responses, we employed the zebrafish caudal fin regeneration models since Ahr activation blocks the regenerative process. Zebrafish regenerate their caudal fins by an orchestrated progression of cell migration, differentiation and proliferation controlled by a multitude of signaling pathways. This complex process was exploited as an in vivo platform to identify cross talk between Ahr and other signaling pathways. Global genomic analysis was performed in the larval regenerating fin tissue after exposure to TCDD in order to identify genes differentially regulated after Ahr activation. Comparative toxicogenomic analysis revealed that both adult and larval fins respond to TCDD during regeneration with mis-expression of Wnt signaling pathway members and Wnt target genes. Experiment Overall Design: The caudal fin of zebrafish larvae at 2days post fertilization were amputated and exposed to vehicle control alone or TCDD. Regenerating fins were isolated at 2and 3 days post amputation. Three replicates were collected at each time point. 150 fins were pooled to comprise one replicate.

2008-04-07 | E-GEOD-10184 | biostudies-arrayexpress

The Aryl Hydrocarbon Receptor Regulates Tissue-Specific Dioxin-Dependent and Dioxin-Independent Gene Batteries

Project description:This SuperSeries is composed of the following subset Series: GSE15857: The Aryl Hydrocarbon Receptor Regulates Tissue-Specific Dioxin-Dependent and Dioxin-Independent Gene Batteries: Kidney GSE15858: The Aryl Hydrocarbon Receptor Regulates Tissue-Specific Dioxin-Dependent and Dioxin-Independent Gene Batteries: Liver Refer to individual Series

2010-05-05 | E-GEOD-15859 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of Uncut and Injured Larval Zebrafish Fin Fold Transcriptomes

Project description:We report increased expression of mitochondrial biogenesis genes in regnerating larval fin fold

2021-08-17 | GSE182113 | GEO

Comparative genomic analysis between adult and larval fin regeneration

Project description:Zebrafish have the remarkable ability to regenerate body parts including the heart, spinal cord and fins by a process referred to as epimorphic regeneration. Recent studies have illustrated that similar to adult zebrafish, early life stage-larvae also possess the ability to regenerate the caudal fin. A comparative genomic analysis was used to determine the degree of conservation in gene expression among the regenerating adult caudal fin, adult heart and larval fin. Results indicate that these tissues respond to amputation/injury with strikingly similar genomic responses. Comparative analysis revealed raldh2, a rate-limiting enzyme for the synthesis of Retinoic acid (RA), as one of the highly induced genes across the three regeneration platforms. Keywords: comparative genomics

2008-02-29 | GSE10188 | GEO

Transcription profiling of zebrafish adult and larval fin to investigate mechanisms of regeneration

2008-04-07 | E-GEOD-10188 | biostudies-arrayexpress

Aryl hydrocarbon receptor-interacting protein regulates tumorigenic and metastatic properties of colorectal cancer cells driving liver metastasis

Project description:Aryl hydrocarbon receptor-interacting protein (AIP), a putative positive intermediary in aryl hydrocarbon receptor-mediated signaling, is overexpressed in highly metastatic human KM12SM CRC cells, with high metastatic capacity to liver, and other highly metastatic CRC cells. Meta-analysis and immunohistochemistry were used to assess the relevance of this protein in CRC. Cellular functions and signaling mechanisms mediated by AIP were assessed by gain-of-function experiments and in vitro and in vivo experiments. A significant association of high AIP expression with poor CRC patients’ survival was observed. Gain-of-function and quantitative proteomics experiments demonstrated that AIP increased tumorigenic and metastatic properties of isogenic KM12C (poorly-metastatic) and KM12SM CRC cells. AIP overexpression dysregulated epithelial-to-mesenchymal (EMT) markers and induced several transcription factors and Cadherin-17 activation. The former induced the signaling activation of AKT, SRC, and JNK kinases to increase adhesion, migration and invasion of CRC cells. In vivo, AIP expressing KM12 cells induced tumor growth and liver metastasis. Furthermore, KM12C (poorly-metastatic) cells ectopically expressing AIP became metastatic to liver. Our data reveal new roles for AIP in regulating proteins associated with cancer and metastasis to induce tumorigenic and metastatic properties in colon cancer cells driving liver metastasis.

2023-05-10 | PXD031119 | Pride

Aryl hydrocarbon receptor dynamically regulates inflammatory and secretory gene pathways in decidual endometrial stromal cells

Project description:We report sequencing of chromatin immunoprecipitated DNA (ChIP-Seq) of Aryl Hydrocarbon Receptor (AHR) targets from decidual stromal cells with kynurenine treatment and normal decidualization media

2019-06-01 | GSE118413 | GEO

Regenerating zebrafish fin fold vs. uncut control

Project description:Teleost fish have the remarkable ability to regenerate their body parts including heart, spinal cord, and the caudal fin, while many higher vertebrates including us humans have only a limited ability. To facilitate molecular and genetic approaches for regeneration, we previously established an assay using the fin fold of early stage larvae, which regenerate their caudal fin folds as in adult regeneration. Here, we performed transcriptional profiling of regenerating larval fin folds and identified genes with differential expression during regeneration. Gene expression profiling of zebrafish larval fin-fold regeneration was performed by comparing amputated fin fold and uncut control. Keywords: Stress response, injury response.

2008-10-01 | GSE11391 | GEO

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