Similar Datasets
Project description:Transcriptional profiling of hdac1 mutant zebrafish in comparison to their sibling embryos. Embryos resulting from a cross between heterozygous hdac1 mutant zebrafish (hi1618/+) where cultured together then mutants separated from the siblings one the basis of phenotype and RNA extracted from the two groups at 27hpf was compared in a two-colour hybridisation.
2011-01-21 | GSE26707 | GEO
Project description:Transcriptional profiling of hdac1 mutant zebrafish in comparison to their sibling embryos. Embryos resulting from a cross between heterozygous hdac1 mutant zebrafish (hi1618/+) where cultured together then mutants separated from the siblings one the basis of phenotype and RNA extracted from the two groups at 27hpf was compared in a two-colour hybridisation. Two-condition experiment, hdac1 mutants vs. sibling. Biological replicates: 2 (separate mating) Technical replicates: 4 (2 of which are dye-swap)
2011-01-21 | E-GEOD-26707 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE26707: Zebrafish 27hpf embryos: hdac1 mutant (hi1618) vs sibling GSE26708: Zebrafish embryos: hdac1 Morphants vs Standard control morphants GSE26709: Zebrafish embryos: hdac1 Morphants vs Standard control morphants at 12, 18 and 27 hpf Refer to individual Series
2011-01-21 | E-GEOD-26710 | biostudies-arrayexpress
Project description:We conducted functional analysis on zebrafish mutant fn10a by polyA+, 100bp paired end, strand-specific RNA-seq. By comparing the transcriptome of fn10a mutants and their wildtype siblings or wildtype controls, we revealed a transcriptome-wide RNA splicing deficiency and a large amount of intron-retaining transcripts, which resulted in compromised nonsense-mediated RNA decay and activation of the p53 pathway in fn10a mutants. 2 biological replicates were performed to consolidate the findings. We also conducted subcellular RNA-seq between fn10a mutants and wildtype siblings, to investigate the localization of intron retaining transcripts.
2017-02-10 | GSE78106 | GEO
Project description:The zebrafish runzel (ruz) carries a mutation in the titin gene resulting in muscle degeneration and embryonic lethality. At the onset of the visible phenotype (3-3.5 days post fertilization), RNA expression of the tail and trunk (primarily skeletal muscle) was compared between ruz mutants and wildtype siblings using the Affymetrix Zebrafish Gene Chip. Mutant RNA was matched with RNA of wildtype siblings from the same clutch. 3 separate clutches were used (n=3). RNA was labeled, sheered, and hybridized as in Shephard et al. (Shepard et al., 2005) and the data analyzed as in Choe et al. and Weber et al. (Choe et al., 2005; Weber et al., 2005). Results suggest a novel mechanism of titin muscular dystrophy pathogenesis including upregulation of heat shock proteins. Experiment Overall Design: At the onset of the visible phenotype (3-3.5 days post fertilization), RNA expression of the tail and trunk (primarily skeletal muscle) was compared between ruz mutants and wildtype siblings using the Affymetrix Zebrafish Gene Chip. RNA of mutants was matched with RNA of wildtype siblings from the same clutch. 3 separate clutches were used (6 arrays total).
2007-10-05 | E-GEOD-4585 | biostudies-arrayexpress
Project description:The neurogenic state at transcriptomic level in delayed-neurogenesis zebrafish mutant "slbp1" with wildtype sibling was compared using bulk RNA sequencing data from RNA obtained from head regions at 2dpf.
2020-03-01 | GSE144517 | GEO
Project description:To understand the role of Pou5f3, Sox19b and Nanog during zebrafish zygotic genome activation, RNA-seq time-series for single, double and triple maternal-zygotic (MZ) zebrafish mutants for Pou5f3, Nanog, Sox19b, as well as the wild-type.
2023-08-02 | GSE162415 | GEO
Project description:Adult sibling homozygous wild type and tcf7l1a mutants were paired and Total RNA was trizol extracted from wild type and maternal zygotic homozygous tcf7l1a mutant embryos at 90% epiboly stage (9 hours post fertilization). ZFIN Identifier ZDB-GENE-980605-30, PMID:11057671. The 3 end of fragmented RNA was pulled down using polyToligos attached to magnetic beads, reverse transcribed, made into Illumina libraries and sequenced using Illumina HiSeq paired-end sequencing. Protocol: Total RNA was extracted from zebrafish embryos using Trizol and DNase treated. Chemically fragmented RNA was enriched for the 3 ends by pulled down using an anchored polyT oligo attached to magnetic beads. An RNA oligo comprising part of the Illumina adapter 2 was ligated to the 5 end of the captured RNA and the RNA was eluted from the beads. Reverse transcription was primed with an anchored polyT oligo with part of Illumina adapter 1 at the 5 end followed by 12 random bases, then an 8 base indexing tags, then CG and 14 T bases. An Illumina library with full adapter sequence was produced by 20 cycles of PCR. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
2014-11-11 | E-ERAD-249 | biostudies-arrayexpress
Project description:We applied time-series SE50bp RNA-seq with 35M reads per sample in wild-type, MZsox19b, MZspg, and double MZspgsox19b mutants in zebrafish embryos to understand the role of Pou5f3 and Sox19b during zebrafish zygotic genome activation. In total we sequenced 4 biological replicates (rep1-4) for WT time curve and 2 biological replicates (rep1-2) for each mutant. WT rep5 are technical replicates for WT rep1, while MZsox19b rep3 and MZspg rep3 are techical replicates for MZsox19b rep1 and MZspg rep1, respectively.
2021-03-03 | GSE137424 | GEO
Project description:Neutrophils are the most abundant vertebrate leukocytes and they are essential to host defense. Despite extensive investigation, the molecular network controlling neutrophil differentiation remains incompletely understood. GFI1 is associated with several myeloid disorders, but its role and the role of its co-regulators in granulopoiesis and pathogenesis are far from clear. Herein, we demonstrate that zebrafish gfi1aa deficiency induces excessive neutrophil progenitor proliferation, accumulation of immature neutrophils from the embryonic stage, and some phenotypes similar to myelodysplasia syndrome in adulthood. Both genetic and epigenetic analysis demonstrated immature neutrophil accumulation in gfi1aa-deficient mutants to be due to up-regulation of cebpα transcription. Increased transcription was associated with Lsd1 altered H3K4 methylation of cebpα regulatory region. Taken together, results demonstrated Gfi1aa, Lsd1, and cebpα to form a regulatory network that controlled neutrophil development, providing a disease progression traceable model for myelodysplasia syndrome. The use of the model will provide new insights into a molecular understanding of GFI1 related myeloid disorders as well a mean by which to develop targeted therapeutic approaches for treatment.
2021-08-20 | GSE182346 | GEO