Slc2a10/glut10 and TBFBR1
Ontology highlight
ABSTRACT:
ORGANISM(S): Danio rerio
SUBMITTER: Seth Crosby
PROVIDER: E-GEOD-34510 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:A zebrafish model of arterial tortuosity syndrome (ATS) was generated by knocking down the slc2a10/glut10 gene using antisense morpholino oligonucleotides (MO). Control morpholino treated embryos were used as controls. The samples were collected for gene expression profiling at 48 hours post fertilization. Experimental details and analyzed data are available in Willaert et al. Human Molecular Genetics 2011; doi: 10.1093/hmg/ddr555 Two-condition experiment, slc2a10 MO (7.5ng) treatment vs control MO (5ng) treatment. Biological replicates: 3 slc2a10 MO replicates, compared to a pooled sample of 3 control MO replicates with dye swap.
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Project description:The zebrafish (Danio rerio) is a popular animal model in studies of vertebrate development and organogenesis. Recent research has shown a similarity of approximately 70% between the human and zebrafish genomes and of 84% in human disease-causing genes, specifically. Zebrafish embryos have a number of desirable features, including transparency, a large size, and rapid embryogenesis. Protein phosphorylation is a well-known post-translational modification (PTM), which performs various biological functions. Recent mass spectrometry (MS) developments have enabled the study of global phosphorylation patterns by using MS-based proteomics coupled with TiO2 phosphopeptide enrichment. In the present study, we identified 3,500 non-redundant phosphorylation sites on 2,166 phosphoproteins and 1,564 quantified phosphoproteins in zebrafish embryos.
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Project description:The zebrafish embryo has repeatedly proved to be a useful model for the analysis of effects by environmental toxicants. This study was performed to investigate if an approach combining mechanism-specific bioassays with microarray techniques can obtain more in-depth insights into the ecotoxicity of complex pollutant mixtures as present, e.g., in freeze-dried whole sediment samples and their corresponding organic extracts in parallel. To this end, altered gene expression was compared to data from established bioassays as well as to results from chemical analysis. Microarray analysis revealed several classes of significantly regulated genes which could to a considerable extent be related to the hazard potential. Results indicate that potential classes of contaminants can be assigned to sediment extracts by both classical biomarker genes and corresponding expression profile analyses of known substances. However, it is difficult to distinguish between specific responses and more universal detoxification of the organism. Additionally, different gene expression was shown to be less influenced by the sampling site than by the method of exposure, which could be attributed to differential bioavailability of contaminants. Microarray analyses were performed with early life stages of zebrafish exposed to sediment extracts or freeze-dried sediment from three sampling sites (Ehingen, Lauchert, Sigmaringen) along the Upper part of the Danube River, Germany. The expression profiles were compared within the sampling sites, between the exposure scheme and to the expression pattern of model toxicants, such as 4-chloroaniline, Cadmium, DDT, TCDD, and Valproic acid (Gene Expression Omnibus Series GSE9357). Additionally, mechanism-specific bioassays and chemical analysis of the sediments have been combined and compared to the present gene expression data.
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Project description:In this study, we found RPS24 is required for both the primitive hematopoiesis and definitive hematopoiesis process partly mediated by P53 pathway. With the RNA-seq and miRNA-seq technique, several deregulated genes and miRNAs were found to be related with hematopoiesis, vascular development and apoptosis process in RPS24-deficient zebrafish. Meanwhile, a comprehensive regulatory network was firstly constructed to indentify the mechanisms of key miRNAs and gene pathways in this Model of Diamond-Blackfan Anemia. Interestingly, we found that the central nodes genes in the network were almost all targeted by significantly deregulated miRNAs, with partial verification from previous studies, revealing that our network-based approach is promising for the identification of new and important miRNAs in DBA. The present study provided comprehensive potential pathogenic genes and miRNAs data that are associated with RPS24-deficient zebrafish embryos as a model of DBA, which should provide a valuable resource for understanding the complex molecular pathogenesis of mutant RPS24-mediated human diseases. Determine the differences of miRNome between RPS24-deficient and MO control zebrafish embryos for understanding the complex molecular pathogenesis of mutant RPS24-mediated human diseases
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