Project description:To determine the molecular basis for the reduced blood cells in circulation in ezh2 mutant zebrafish, we performed high-throughput sequencing at 28 hpf. Results revealed 893 up-regulated genes and 425 down-regulated genes in the ezh2 mutant zebrafish compared with wild-type zebrafish. We found that some hematopoietic genes are down-regulated in ezh2 mutant zebrafish, which was reconfirmed with qRT-PCR.
Project description:Goal of the experiment was to assess the differences in gene expression between maternal zygotic ezh2 mutant zebrafish embryos and wildtype embryos at 0 and 3.3 hpf.
Project description:Overexpression of EZH2 in estrogen receptor negative (ER-) breast cancer promotes metastasis. EZH2 has been mainly studied as the catalytic component of the Polycomb Repressive Complex 2 (PRC2) that mediates gene repression by trimethylating histone H3 at lysine 27 (H3K27me3). However, how EZH2 drives metastasis despite the low H3K27me3 levels observed in ER- breast cancer is unknown. We have shown that in human invasive carcinomas and distant metastases, cytoplasmic EZH2 phosphorylated at T367 is significantly associated with ER- disease and low H3K27me3 levels. Here, we explore the interactome of EZH2 and of a phosphodeficient mutant EZH2_T367A. We identified novel interactors of EZH2, and identified interactions that are dependent on the phosphorylation and cellular localization of EZH2 that may play a role in EZH2 dependent metastatic progression.
Project description:Polycomb group (PcG) proteins are transcriptional repressors important to maintain cell identity during embryonic development. Ezh2, the catalytic subunit of the Polycomb Repressive Complex 2, is responsible for placing the epigenetic repressive mark histone H3 lysine 27 trimethylation (H3K27me3). In contrast to results in mouse models, zebrafish embryos mutant for both maternal and zygotic ezh2 (MZezh2) can form a normal body plan at 1 day post fertilization (dpf) but die at 2 dpf, exhibiting pleiotropic phenotypes. To elucidate the specificity of PcG-mediated repression during early zebrafish development, we conducted in depth analysis of the transcriptome, epigenome, and proteome of the MZezh2 mutant embryos at 1 dpf. We found that, despite modifications in the epigenetic landscape, transcriptome and proteome analysis revealed only minor changes in gene and protein expression levels.
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.
Project description:Purpose: To explore the mechanism of how Tan I inhibits malignant hematopoiesis at the gene expression level Methods: 72 hpf Tg(c-mybhyper: GFP) zebrafish embryos treated with DMSO or Tan I 60 μM were collected for RNA sequencing Results: We found that 1882 genes were differentially expressed between DMSO and Tan I treatment in c-mybhyper fish embryos (p value <=0.05, |log2 fold change| >= 0.25) Conclusions: We identified MMP9 and ABCG2 as two possible downstream genes of Tan I’s effects on EZH2
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