Expression profiling of LSK cells from Bmi1 cKO mice in hematopoiesis versus LSK control cells from WT mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE31404 | GEO | 2011/10/30
SECONDARY ACCESSION(S): PRJNA145729
REPOSITORIES: GEO
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Project description:Bmi1 is a protein member of PRC1 and plays a major role in the maintenance of gene repression. We are studying the role of Bmi1 in the context of hematopoietic stem cell aging. We used microarray to study the gene expression profile of LSK cells in relation to the knocking-out of Bmi1 in vivo LSK cells were labeled using antibodies against specific surface markers and isolated by fluorescence-activated cell sorting in trizol.
2011-10-29 | E-GEOD-31404 | biostudies-arrayexpress
Project description:Identification of BMI1, RYBP and H2AK119UB interactome in Glioblastoma (GBM) to elucidate BMI1 roles independent of the PRC1-complex in GBM.
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Project description:Glioblastoma (GBM) is the most common and aggressive intrinsic brain tumour in adults. Epigenetic mechanisms controlling normal brain development are often dysregulated in GBM. Among these, BMI1, a structural component of the Polycomb Repressive Complex 1 (PRC1), which promotes the H2AK119ub catalytic activity of Ring1B, is upregulated in GBM and its tumorigenic role has been shown in vitro and in vivo. Here, we have used protein and chromatin immunoprecipitation followed by mass spectrometry (MS) analysis to elucidate the protein composition of PRC1 in GBM and CRISPR/dCAS9-mediated modulation of BMI1 to assess its influence on protein interactions. We show that while well-established BMI1 functions such as control of cell proliferation and cell adhesion are PRC1-dependent, novel regulatory functions in mRNA splicing and cholesterol transport are PRC1 independent and may represent novel targetable mechanisms in GBM.
2021-03-04 | GSE159747 | GEO
Project description:Mammalian spermatogenesis is regulated by epigenetic mechanisms that maintain cell type-specific transcriptional programs. The epigenetic regulator BMI1, a PRC1 member, is required for maintaining undifferentiated spermatogonia, but the underlying mechanisms remain unclear. To address this issue, here we performed RNA-sequencing (RNA-seq) analysis in both wild type and Bmi1 knockdown spermatogonia populations.
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Project description:EBV proteins EBNA3A, EBNA3B and EBNA3C control hundreds of host genes after infection. Changes in epigenetic marks around EBNA3-regulated genes suggest they exert transcriptional control in collaboration with epigenetic factors. The roles of PRC2 subunit SUZ12 and of PRC1 subunit BMI1 were assessed for their importance in EBNA3-mediated repression and activation. ChIP-seq experiments for SUZ12 and BMI1 were performed to determine their global localization on chromatin and analysis offered further insight into polycomb protein distribution in differentiated cells. Their localization was compared to that of each EBNA3, to resolve longstanding questions about the EBNA3-polycomb relationship. SUZ12 did not co-localize with any EBNA3, whereas EBNA3C co-localized significantly and co-immunoprecipitated with BMI1. In cells expressing a conditional EBNA3C, BMI1 was sequestered to EBNA3C binding sites after EBNA3C activation. When SUZ12 or BMI1 was knocked down in the same cells, SUZ12 did not contribute to EBNA3C-mediated regulation. Surprisingly, after BMI1 knock down, EBNA3C repressed equally efficiently, but host gene activation by EBNA3C was impaired. This overturns previous assumptions about BMI1/PRC1 functions during EBNA3C-mediated regulation, for the first time identifies directly a host factor involved in EBNA3-mediated activation and provides a new insight of how PRC1 can be involved in gene activation.
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Project description:Purpose: Study of the role of BMI1 dependent and indpendent of PRC1 in castration-resistant prostate cancer(CRPC) Method: The expression of BMI1 or RING1B was silenced by 2 independent siRNA strands targeted at BMI1 or RING1B in C4-2 cells, scramble RNA as control. mRNA profiles and genome-wide chromatin-state maps were generated by deep sequencing. AR, BMI1 and IgG ChIP was conducted in C4-2 cells. Results: AR-induced genes were significantly down regulated by BMI1 knockdown but not RING1B. higher expression levels of BMI1 activated genes (those downregulated by BMI1 knockdown) were significantly associated with poorer disease-free and poorer overall survival.
2018-02-07 | GSE97831 | GEO
Project description:FOXP3+ Treg cells are expanded within the inflamed intestine of human Crohn’s disease, yet FOXP3-mediated gene repression within these cells is lost. The Polycomb repressive complexes play a role in FOXP3 target gene regulation, but deeper mechanistic insight is incomplete. We have now specifically identified the Polycomb Repressive Complex 1 (PRC1) family member, BMI1 in the regulation of a pro-inflammatory enhancer network in both human and murine Tregs. Using human Tregs and lamina propria T cells, we inferred PRC1 to regulate Crohn’s associated gene networks through assays of chromatin accessibility. Conditional deletion of BMI1 in murine FOXP3+ cells led to systemic inflammation. BMI1-deficient Tregs beared a TH1/TH17-like phenotype as assessed by assays of genome wide transcription, chromatin accessibility and proteomic techniques. Finally, BMI1 mutant FOXP3+ cells did not suppress colitis in the adoptive transfer model of human inflammatory bowel disease. We propose that BMI1 plays an important role in enforcing Treg identity in vitro and in vivo. Loss of Treg identity via genetic or transient BMI1 depletion perturbs the epigenome and converts Tregs into Th1/Th17-like proinflammatory cells, a transition relevant to human Crohn’s disease associated CD4+ T cells.
2021-03-31 | GSE171189 | GEO
Project description:Mammalian spermatogenesis is regulated by epigenetic mechanisms that maintain cell type-specific transcriptional programs. The epigenetic regulator BMI1, a PRC1 member, is required for maintaining undifferentiated spermatogonia, but the underlying mechanisms remain unclear. To address this issue, here we performed chromatin immunoprecipitation followed by massive parallel sequencing (ChIP-seq).
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Project description:FOXP3+ Treg cells are expanded within the inflamed intestine of human Crohn’s disease, yet FOXP3-mediated gene repression within these cells is lost. The Polycomb repressive complexes play a role in FOXP3 target gene regulation, but deeper mechanistic insight is incomplete. We have now specifically identified the Polycomb Repressive Complex 1 (PRC1) family member, BMI1 in the regulation of a pro-inflammatory enhancer network in both human and murine Tregs. Using human Tregs and lamina propria T cells, we inferred PRC1 to regulate Crohn’s associated gene networks through assays of chromatin accessibility. Conditional deletion of BMI1 in murine FOXP3+ cells led to systemic inflammation. BMI1-deficient Tregs beared a TH1/TH17-like phenotype as assessed by assays of genome wide transcription, chromatin accessibility and proteomic techniques. Finally, BMI1 mutant FOXP3+ cells did not suppress colitis in the adoptive transfer model of human inflammatory bowel disease. We propose that BMI1 plays an important role in enforcing Treg identity in vitro and in vivo. Loss of Treg identity via genetic or transient BMI1 depletion perturbs the epigenome and converts Tregs into Th1/Th17-like proinflammatory cells, a transition relevant to human Crohn’s disease associated CD4+ T cells.
2021-03-31 | GSE171188 | GEO
Project description:FOXP3+ Treg cells are expanded within the inflamed intestine of human Crohn’s disease, yet FOXP3-mediated gene repression within these cells is lost. The Polycomb repressive complexes play a role in FOXP3 target gene regulation, but deeper mechanistic insight is incomplete. We have now specifically identified the Polycomb Repressive Complex 1 (PRC1) family member, BMI1 in the regulation of a pro-inflammatory enhancer network in both human and murine Tregs. Using human Tregs and lamina propria T cells, we inferred PRC1 to regulate Crohn’s associated gene networks through assays of chromatin accessibility. Conditional deletion of BMI1 in murine FOXP3+ cells led to systemic inflammation. BMI1-deficient Tregs beared a TH1/TH17-like phenotype as assessed by assays of genome wide transcription, chromatin accessibility and proteomic techniques. Finally, BMI1 mutant FOXP3+ cells did not suppress colitis in the adoptive transfer model of human inflammatory bowel disease. We propose that BMI1 plays an important role in enforcing Treg identity in vitro and in vivo. Loss of Treg identity via genetic or transient BMI1 depletion perturbs the epigenome and converts Tregs into Th1/Th17-like proinflammatory cells, a transition relevant to human Crohn’s disease associated CD4+ T cells.
2021-03-31 | GSE171187 | GEO