Zebrafish metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA327716 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:zebrafish Genome sequencing and assembly
| PRJNA327784 | ENA
Project description:Using a pooled (n=10) zebrafish liver DNA, we generated base-resolution DNA methylation maps to document epigenetic landscape in zebrafish genome. Here we generated single-nucleotide resoultion DNA methylation map of zebrafish pooled liver sample using Reduced Representation Bisulfite Sequencing (RRBS)
2014-10-01 | E-GEOD-59917 | biostudies-arrayexpress
Project description:With the emergence of zebrafish as an important model organism, a concerted effort has been made to study its transcriptome. This effort is limited by gaps in zebrafish annotation, which is especially pronounced concerning transcripts dynamically expressed during zygotic genome activation (ZGA). To date, short read sequencing has been the principal technology for zebrafish transcriptome annotation. In part because these sequence reads are too short for assembly methods to resolve the full complexity of the transcriptome, the current annotation is rudimentary. By providing direct observation of full-length transcripts, recently refined long-read sequencing platforms can dramatically improve annotation coverage and accuracy. Here, we leveraged the SMRT platform to study the early ZGA-stage zebrafish transcriptome. Our analysis revealed additional novelty and complexity in the zebrafish transcriptome, identifying 2748 high confidence novel transcripts that originated from previously unannotated loci and 1835 new isoforms in previously annotated genes.
2018-05-24 | GSE101843 | GEO
Project description:During development, the inherited DNA methylation patterns from the parental gametes needs to be remodeled into a state compatible with embryonic pluripotency. In Zebrafish, this remodeling is achieved by the maternal methylome becoming hypomethylated to match the paternal methylome. However, how this is achieved in medaka (another teleost fish) is currently not known. Moreover, how DNA methylation remodeling is impacted in hybrid organisms, and the effects this may have on their development, is also not known. Here we address these questions by generation whole genome bisulfite sequencing data for zebrafish, medaka and zebrafish medaka embryos.
2023-08-25 | E-MTAB-12535 | biostudies-arrayexpress
Project description:Genome-wide analysis of H3K4me3 modifications, Gata1 binding, and DNase I hypersensitivity sites in zebrafish adult red blood cells Zebrafish peripheral blood nuclei were isolated for DNase I hypersensitivity assays. Total DNA were purified using the Proteinase K digestion and Phenol-Chloroform extraction. Small DNase I fragments from the DNaseI treatement were enriched using a sucrose gradient. These ends were then labeled and amplified during library construction and for Solexa sequencing
2012-02-17 | E-GEOD-35875 | biostudies-arrayexpress
Project description:The proteome of human brain synapses is highly complex and mutated in over 130 diseases. This complexity arose from two whole genome duplications early in the vertebrate lineage. Zebrafish are used in modelling human diseases, however its synapse proteome is uncharacterised and whether the teleost-specific genome duplication (TSGD) influenced complexity is unknown. We report the first characterisation of the proteomes and ultrastructure of central synapses in zebrafish and analyse the importance of the TSGD. The TSGD increased overall synapse proteome complexity. The Post Synaptic Density (PSD) proteome of zebrafish had lower complexity than mammals and a highly conserved set of ~1000 proteins is shared across vertebrates. PSD ultrastructural features were also conserved. Lineage-specific proteome differences indicate vertebrate species evolved distinct synapse types and functions. The datasets are a resource for a wide range of studies and have important implications for the use of zebrafish in modelling human synaptic diseases.
2017-03-06 | PXD005630 | Pride
Project description:Hypoplastic left heart syndrome (HLHS) is characterized by underdevelopment of left sided structures including the ventricle, valves, and aorta1. Although the mechanisms of disease pathogenesis remain elusive due to a paucity of candidate genes and animal models, prevailing paradigm suggests that HLHS is a multigenic disease of co-occurring phenotypes2,3. Here, we report that zebrafish lacking two orthologs of the RNA binding protein RBFOX2, a gene previously linked to HLHS in humans4,5, display cardiovascular defects overlapping those in HLHS patients. In contrast to current models, we demonstrate that co-existing ventricular, valve, and aortic deficiencies in rbfox mutant zebrafish arise secondary to impaired myocardial function as all three phenotypes are rescued when Rbfox is expressed specifically in the myocardium. On a molecular and cellular level, we find diminished expression and alternative splicing of sarcomere and mitochondrial components in rbfox-deficient hearts that compromise sarcomere assembly and mitochondrial respiration, respectively. Injection of human RBFOX2 mRNA restores ventricular structure and function in rbfox mutant zebrafish, while HLHS-linked RBFOX2 variants fail to rescue. Taken together, our data suggest that mutations in RBFOX2 are causal for HLHS pathogenesis and provide a complimentary paradigm for HLHS emergence where co-existing ventricular, valve, and aortic deficiencies have a monogenic etiology caused by myocardial dysfunction.
2022-07-12 | MTBLS4176 | MetaboLights