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Histone modifications in livers from wild-type male and female mice, and in livers from mice with a Double Knockout (DKO) of Ezh1 and Ezh2

ABSTRACT: Histone modifications in livers from wild-type male and female mice, and in livers from mice with a Double Knockout (DKO) of Ezh1 and Ezh2

PROVIDER: PRJNA434742 | ENA |

REPOSITORIES: ENA

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Histone modifications in livers from wild-type male and female mice, and in livers from mice with a Double Knockout (DKO) of Ezh1 and Ezh2

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.

2020-04-28 | GSE110887 | GEO

RNA-seq gene expression profiling of livers from wild-type male and female mice, and from mice with a Double Knockout (DKO) of Ezh1 and Ezh2.

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

2020-04-28 | GSE110879 | GEO

RNA-seq gene expression profiling of livers from wild-type male and female mice, and from mice with a Double Knockout (DKO) of Ezh1 and Ezh2.

Project description:RNA-seq gene expression profiling of livers from wild-type male and female mice, and from mice with a Double Knockout (DKO) of Ezh1 and Ezh2.

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Expression data from LSK cells from mice with knock-out of Ezh1 versus LSK control

Project description:Ezh1 is a protein member of PRC2. Ezh1 has been described as a functional repressor gene, such as its homologous Ezh2. We are investigating the role of Ezh1 in hematopoietic stem cells, aging, self-renewal and differentiation. We used microarrays to detail the global program of gene expression in LSK cells from mice with knocked-down expression of Ezh1. LSK cells from EZH1 knockout and control mice were marked and isolated by fluorescence-activated cell sorting. 2 replicates each.

2012-03-06 | E-GEOD-36288 | biostudies-arrayexpress

Divergent mechanisms of EZH1 regulation of heart development and regeneration [RNA-Seq]

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

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Coordinated activities of EZH2 and EZH1 are essential for neurogenesis

Project description:Polycomb group proteins (PcG) are well known by their function in the regulation of developmental processes. PcG mediated regulation of genetic programs required for proper development are triggered by EZH2 H3K27 methyltransferase activity. EZH1 can partially substitute EZH2 activity. However, unlike EZH2, EZH1 is presence in differentiated and adult tissues suggesting additional biological functions. Here we show that EZH2 is predominantly expressed in neural stem cells being essential for neural stem cells self renewal and homeostasis. There, it controls the transcriptional state of cell cycle regulators, such as CIP1. But it is also necessary to regulate genes involved in surveillance and neuroepithelial polarity. In contrast, EZH1 expression is more abundant in differentiated cells within the spinal cord and its downregulation unables neural stem cells to differentiate. All together our data reveal a complementary but non-redundant role of EZH2 and EZH1 in neurogenesis.

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mRNA-seq of ARID1B KO and ARID1A/1B DKO livers

Project description:mRNA-seq of ARID1B KO and ARID1A/1B DKO livers

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The Quantitative Analysis of Transcriptomes Derived From Ezh2- or Ezh1/2-Deleted Leukemia Stem Cells of Murine Acute Myloid Leukemia

Project description:We report dual genetic delstion of Ezh1/2 in murine AML model induced cell cyle progression of quiescent LSCs and cell differentiation of LSCs. To investigate the underlying mechanism by which Ezh1/2 regulate quiescent LSCs and maintein the stemness of LSCs, we performed RNA sequencing of L-GMPs derived from Ezh2- and Ezh1/2-deleted AML mice.

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Expression data from LSK cells from mice with knock-out of Ezh1 versus LSK control

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Loss of EZH2 results in enhanced recruitment of EZH1, Pol II and Stat5 and precocious mammary gland development

Project description:Establishment and differentiation of mammary alveoli during pregnancy are controlled by prolactin through the transcription factor STAT5. As pregnancy progresses mammary signature genes are activated in a defined temporal order, which coincides with the recruitment of STAT5 to respective regulatory sequences. This study addressed the question whether the methyltransferase and transcriptional co-activator EZH2 controls the differentiation clock of mammary epithelium. Ablation of Ezh2 from mammary stem cells resulted in precocious differentiation of alveolar epithelium and accelerated activation of mammary signature genes. This coincided with enhanced occupancy by EZH1, Pol II and STAT5 to mammary-specific loci. Notably, loss of EZH2 did not result in overt changes in genome-wide and gene-specific H3K27me3 patterns, suggesting that enhanced EZH1 recruitment can compensate for the loss of EZH2. However, differentiated mammary epithelia failed to form in the combined absence of EZH1 and EZH2. Transplantation experiments failed to demonstrate a role for EZH2 in the biology of mammary stem and progenitor cells. In summary, while EZH1 and EZH2 serve redundant functions in the establishment of H3K27me3 and formation of mammary alveoli, the presence of EZH2 is required to obtain controlled temporal differentiation of mammary epithelium. ChIP-seq EZH1, EZH2, PolIII; WT and E2KO mammary cells

2015-01-27 | E-GEOD-65284 | biostudies-arrayexpress

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