Project description:Transcription profiling by array of striatal tissue of wild type and Ezh1/Ezh2 double knockout mice at 6 weeks, 3 months, and 6 months
Project description:Transcriptomic (RNA-seq) analysis of wild-type and Nolz1-/- (Zfp503) mutant striatal tissue reveals altered expression of several genes involved in striatal projection neuron specification.
Project description:We analyzed the genomic distribution of H3K27me3 in a clone of c-Myc iMEFs (clone C2) either i) wild-type for Ezh2, ii) in the presence of overexpressed exogenous Ezh2, iii) Ezh2-mutant, and iv) Ezh1/Ezh2 pre-deletion (Ezh1/Ezh2 introduced before deletion of endogenous Ezh2) and Ezh2 post-deletion rescue (Ezh2 re-introduced in Ezh2-mutant cells).
Project description:Chromatin immunoprecipitation and sequencing for 3 histone marks (H3K27ac, H3K27me3 and H3K4me1) was performed on livers of male and female mice with a combined loss of Ezh1 and Ezh2. The DKO mouse model used in these analyses is a global deletion of Ezh1 and hepatocyte-specific deletion of Ezh2, and is described in Bae WK et al, FASEB J. 2015 May;29(5):1653-62. doi: 10.1096/fj.14-261537. PMID: 25477280.
Project description:Polycomb group (PcG) proteins initiate the formation of repressed chromatin domains and regulate developmental gene expression. A mammalian PcG protein, Enhancer of Zeste homolog 2 (Ezh2), triggers transcriptional repression by catalyzing the addition of methyl groups onto lysine-27 of histone H3 (H3K27me2/3)1. This action facilitates the binding of other PcG proteins to histone H3 and compaction of chromatin. Interestingly, there exists a paralog of Ezh2, termed Ezh1, whose primary function remains unclear. Here, we provide evidence for genome-wide association of Ezh1 with active epigenetic marks, RNA polymerase II (PolII) and mRNA production. Ezh1 depletion reduced global PolII occupancy within gene bodies and resulted in delayed transcriptional activation during differentiation of skeletal muscle cells. Conversely, ectopic expression of wild-type Ezh1 led to premature gene activation and rescued PolII-elongation defects in Ezh1-depleted cells. Collectively, these findings reveal an unanticipated role of a PcG protein in promoting mRNA transcription. Examination of 3 different histone modifications, 3 modified forms of RNA polymerase II, Ezh1, Ezh2 and mRNA levels in a skeletal muscle cells at various developmental stages.
Project description:Microarray for duodenum epithelium of C57Bl6 PPARgVillinCRE and wild type mice submitted to 2 weeks 75% caloric restriction compared to ad libitum fed controls
Project description:RNA-seq for DKO, E1KO, E2KO and WT E12.5 heart revealed that EZH1 and EZH2 play a partially redundant role to trimethylate histone H3 at Lys 27 (H3K27me3). Through EZH1, H3K27me3 and H3K27ac ChIP-seq and RNA-seq for P13 EZH1 and GFP overexpressing heart (AAVEzh1 and AAVGFP respectively) suffered MI at P10, we surprisingly found that EZH1 can active the expression of regenerating relevant genes by directly binding to the promoter of targeted genes and through a mechanism independent of H3K27me3 deposition. Together, we unravel a requirement but divergent mechanisms of EZH1 in heart development and regeneration
Project description:PolyA-selected RNA isolated from livers of adult male and female mice with a combined loss of EZH1 and EZH2 in hepatocytes was analyzed by RNA-seq. The DKO mouse model used in these analyses is a global deletion of Ezh1 and hepatocyte-specific deletion of Ezh2, and is described in Bae WK, Kang K, Yu JH, Yoo KH, Factor VM, Kaji K, Matter M, Thorgeirsson S, Hennighausen L. FASEB J. 2015 May;29(5):1653-62. doi: 10.1096/fj.14-261537. PMID: 25477280
