Danio rerio
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA209714 | ENA |
REPOSITORIES: ENA
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Project description:The morphogen Sonic H edgehog governs a wide range of developmental processes. The zebrafish genetic mutant iguana has vascular stability defects due to decreased Shh signaling. Using iguana mutant embryos and embryos treated with the Hedgehog pathway inhibitor cyclopamine, we conducted a microarray to determine genes that are specifically regulated by Shh signaling, and that might mediate vascular stability. We populate a list of 40 genes to have significantly altered expression in both conditions. Using in situ hybridization and quantitative real-time PCR, we verify the expression changes seen in a subset of genes from the list and determine their localization during embryonic development. We then assay the functional relevance of one of the array hits, the cell-cycle regulator pim1, which was upregulated on the microarray. By overexpressing pim1, we observe a loss of vascular stability, similar to that of iguana mutants. Furthermore, chemical inhibition of pim1 in iguana mutant embryos or cyclopamine treated embryos rescues vascular stability. We conclude that the microarray identified a set of genes that are differentially expressed in two distinct modes of Shh signaling interference. Furthermore, this set of genes contains a high proportion of factors potentially involved in vascular stabilization. The identification of these genes is the first step in defining the molecular mechanism by which Shh promotes vascular stability. 3 biological cyclopamine treated samples plus 3 biological DMSO treated controls, plus 3 biological replicates of iguana mutants plus 3 wild type sibling controls, all collected at 30 hpf
2014-06-30 | E-GEOD-48335 | biostudies-arrayexpress
Project description:Purpose: The goals of this study are to investigate the toxic effects and molecular mechanisms of GO exposure in adult zebrafish liver by transcriptome profiling (RNA-seq) Methods: Liver mRNA profiles of three-month-old control (CK) and GO-exposed (GO) zebrafish were generated by deep sequencing, in triplicate, using Illumina Hiseq X ten. The sequence reads that passed quality filters were analyzed at the gene level with two methods: RSEM and HISAT followed by Ballgown. qRT-PCR validation was performed using SYBR Green assays Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the zebrafish genome (GRCz11) and identified 43,106 genes in the livers of CK and GO zebrafish with RSEM and HISAT2 workflow. RNA-seq data confirmed stable expression of 10 known housekeeping genes, and 6 of these were validated with qRT-PCR. Approximately 0.7% of the genes showed differential expression between the CK and GO liver, with a fold change ≥1.5 and p value <0.05. Hierarchical clustering of differentially expressed genes uncovered several genes that may contribute to function in liver inflammation and lipid disorder. Conclusions: Our study represents the detailed analysis of zebrafish liver transcriptomes after GO exposure, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that steroid hormone biosynthesis, lipoprotein metabolic process and PPAR signaling pathway were signifificantly enriched. Most of the lipid metabolism genes were down-regulated while majority of the immune genes were up-regulated after GO treatment.
2020-02-24 | GSE145760 | GEO
Project description:Natural Variation in Fish Transcriptomes: Comparative Analysis of the Zebrafish (Danio rerio)
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Project description:The morphogen Sonic H edgehog governs a wide range of developmental processes. The zebrafish genetic mutant iguana has vascular stability defects due to decreased Shh signaling. Using iguana mutant embryos and embryos treated with the Hedgehog pathway inhibitor cyclopamine, we conducted a microarray to determine genes that are specifically regulated by Shh signaling, and that might mediate vascular stability. We populate a list of 40 genes to have significantly altered expression in both conditions. Using in situ hybridization and quantitative real-time PCR, we verify the expression changes seen in a subset of genes from the list and determine their localization during embryonic development. We then assay the functional relevance of one of the array hits, the cell-cycle regulator pim1, which was upregulated on the microarray. By overexpressing pim1, we observe a loss of vascular stability, similar to that of iguana mutants. Furthermore, chemical inhibition of pim1 in iguana mutant embryos or cyclopamine treated embryos rescues vascular stability. We conclude that the microarray identified a set of genes that are differentially expressed in two distinct modes of Shh signaling interference. Furthermore, this set of genes contains a high proportion of factors potentially involved in vascular stabilization. The identification of these genes is the first step in defining the molecular mechanism by which Shh promotes vascular stability.
2014-06-30 | GSE48335 | GEO
Project description:Mtx2 dependent genes during Zebrafish gastrulation
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