Microarray analysis of Mef2c deficient and control bone marrow pre-B and pro-B cells
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PROVIDER: PRJNA269749 | ENA |
REPOSITORIES: ENA
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Project description:Gene expression of mice bone marrow pro-B cells from both control and Vav-Cre Mef2cfl/fl mice (9 months old) We used these microarrays to identify the function of MEF2C in BM B lymphoid progenitors
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Project description:Gene expression of mice bone marrow pre-B cells from both control and Vav-Cre Mef2cfl/fl mice (9 months old) We used these microarrays to identify the function of MEF2C in BM B lymphoid progenitors
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Project description:This SuperSeries is composed of the SubSeries listed below.
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Project description:Acute myelogenous leukemia (AML) is driven by leukemic stem cells (LSC) generated by mutations that confer (or maintain) self-renewal potential coupled to an aberrant differentiation program. Using retroviral mutagenesis, we identified genes that generate LSC in collaboration with genetic disruption of the gene encoding interferon response factor 8 (Irf8), which induces a myeloproliferation in vivo. Amongst the targeted genes, we identified Mef2c, encoding a MADS transcription factor, and confirmed that over-expression induced a myelomonocytic leukemia in cooperation with Irf8 deficiency. Strikingly, several of the genes identified in our screen have been reported to be upregulated in the mixed-lineage leukemia (MLL) subtype. High MEF2C expression levels were confirmed in AML patient samples with MLL gene disruptions, prompting an investigation of the causal interplay. Using a conditional mouse strain, we demonstrated that Mef2c deficiency does not impair the establishment nor maintenance of LSC generated in vitro by MLL/ENL fusion proteins â?? however, its loss led to compromised homing and invasiveness of the tumor cells. Mef2c-dependent targets included several genes encoding matrix metalloproteinases and chemokine ligands and receptors, providing a mechanistic link to increased homing and motility. Thus an early event in LSC generation may be responsible for the aggressive nature of this leukemia subtype. Experiment Overall Design: For gene expression profiling of M/E cells, RNA was isolated from M/E-Mef2c del/- cells infected with MYs-iPAC (empty vector) or MYs-pMef2cASR after puromycin selection at three different time points, pooled, and hybridized against the Agilent Whole Mouse Genome Microarray 4x44K using the one-color service of Miltenyi. Transcript levels were verified by real-time RT-PCR using the SYBRGreen Reaction Mix (Roche Mannheim) in a Roche Light-Cycler. cDNA levels were normalized against Hprt transcript levels. Primers and amplification conditions are available upon request.
2009-08-15 | E-GEOD-17231 | biostudies-arrayexpress
Project description:We analyzed the chromatin accessibility of control and Mef2c deficient mouse BM pre-B and myeloid cells by ATAC-seq analysis.
2016-07-12 | GSE81508 | GEO
Project description:Acute myelogenous leukemia (AML) is driven by leukemic stem cells (LSC) generated by mutations that confer (or maintain) self-renewal potential coupled to an aberrant differentiation program. Using retroviral mutagenesis, we identified genes that generate LSC in collaboration with genetic disruption of the gene encoding interferon response factor 8 (Irf8), which induces a myeloproliferation in vivo. Amongst the targeted genes, we identified Mef2c, encoding a MADS transcription factor, and confirmed that over-expression induced a myelomonocytic leukemia in cooperation with Irf8 deficiency. Strikingly, several of the genes identified in our screen have been reported to be upregulated in the mixed-lineage leukemia (MLL) subtype. High MEF2C expression levels were confirmed in AML patient samples with MLL gene disruptions, prompting an investigation of the causal interplay. Using a conditional mouse strain, we demonstrated that Mef2c deficiency does not impair the establishment nor maintenance of LSC generated in vitro by MLL/ENL fusion proteins – however, its loss led to compromised homing and invasiveness of the tumor cells. Mef2c-dependent targets included several genes encoding matrix metalloproteinases and chemokine ligands and receptors, providing a mechanistic link to increased homing and motility. Thus an early event in LSC generation may be responsible for the aggressive nature of this leukemia subtype.
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Project description:The Mef2 family transcriptional regulator Mef2c is highly expressed in maturing bone marrow and peripheral mature B cells. To evaluate the role of this transcription factor in B cell development, we generated a B cell specific conditional deletion of Mef2c using the Mb-1-Cre transgene that is expressed during the early stages of immunoglobulin rearrangement. Young mice possessing this defect demonstrated a significant impairment in B cell numbers in bone marrow and spleen. This phenotype was evident in all B cell subsets; however, as the animals mature, the deficit in the peripheral mature B cell compartments was overcome. The absence of Mef2c in mature B cells led to unique CD23+ and CD23- subsets that were evident in Mef2c KO primary samples as well as cultured, differentiated B cells but not in WT cell populations. Genome wide expression analysis of immature and mature B cells lacking Mef2c indicated altered expression for a number of key regulatory proteins for B cell function including Ciita, CD23, Cr1/Cr2, and Tnfsf4. Chromatin immunoprecipitation analysis confirmed Mef2c binding to the promoters of these genes indicating a direct link between the presence (or absence) of Mef2c and altered transcriptional control in mature B cells. Four samples are submitted.
2012-05-31 | E-GEOD-34210 | biostudies-arrayexpress
Project description:The Mef2 family transcriptional regulator Mef2c is highly expressed in maturing bone marrow and peripheral mature B cells. To evaluate the role of this transcription factor in B cell development, we generated a B cell specific conditional deletion of Mef2c using the Mb-1-Cre transgene that is expressed during the early stages of immunoglobulin rearrangement. Young mice possessing this defect demonstrated a significant impairment in B cell numbers in bone marrow and spleen. This phenotype was evident in all B cell subsets; however, as the animals mature, the deficit in the peripheral mature B cell compartments was overcome. The absence of Mef2c in mature B cells led to unique CD23+ and CD23- subsets that were evident in Mef2c KO primary samples as well as cultured, differentiated B cells but not in WT cell populations. Genome wide expression analysis of immature and mature B cells lacking Mef2c indicated altered expression for a number of key regulatory proteins for B cell function including Ciita, CD23, Cr1/Cr2, and Tnfsf4. Chromatin immunoprecipitation analysis confirmed Mef2c binding to the promoters of these genes indicating a direct link between the presence (or absence) of Mef2c and altered transcriptional control in mature B cells.
2012-06-01 | GSE34210 | GEO
Project description:Ebf1 deficient pre-pro B-cells (Fraction A) can be cultured in the presence of stromal feeders and cytokines. The retroviral transduction of these cells with Ebf1 was used as gain-of-function experiment for the analysis of direct and functional target genes of Ebf1. Ebf1 deficient pre-pro B-cells were retrovirally transduced with an Ebf1-expressing or control retrovirus. 24h after transduction the infected cells were isolated and their gene expression profile was compared.
2010-07-29 | E-GEOD-21455 | biostudies-arrayexpress
Project description:Ebf1 deficient pre-pro B-cells (Fraction A) can be cultured in the presence of stromal feeders and cytokines. The retroviral transduction of these cells with Ebf1 was used as gain-of-function experiment for the analysis of direct and functional target genes of Ebf1.
2010-06-24 | GSE21455 | GEO