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C/EBPepsilon ChIP-sequencing of C57BL/6 mice bone marrow cells

ABSTRACT: To characterize the genome wide C/EBPepsilon binding sites, ChIP-sequencing with C57BL/6 mice bone marrow cells were performed. To prevent artifact from PCR amplifiation, sequencing or antibody specificity, two controls of input DNA and ChIP-sequencing of C/EBPepsilon knock-out bone marrow cells were used. Two data sets derived from two anti-C/EBPepsilon antibodies, N-terminal (GTX109155) and C-terminal (SC-158) antibody against wild type and C/EBPepsilon knock-out bone marrow cells were generated.

ORGANISM(S): Mus musculus

PROVIDER: GSE73844 | GEO | 2017/06/02

SECONDARY ACCESSION(S): PRJNA298234

REPOSITORIES: GEO

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Project description:Somatic mutation in the X-linked phosphatidylinositol glycan class A (PIG-A) gene causes glycosylphosphatidylinositol (GPI) anchor deficiency in humans with Paroxysmal Nocturnal Hemoglobinuria (PNH). Clinically, patients with PNH have intravascular hemolysis, venous thrombosis and bone marrow failure. We produced a conditional Pig-a knock-out mouse model specifically inactivating the Pig-a gene in hematopoietic cells to study the role of PIG-A deficiency in PNH pathophysiology. We used Affymetrix Mouse Genome 430 2.0 chips to investigate the gene expression pattern in the mouse model of targeted Pig-a deletion. Experiment Overall Design: We performed microarray analysis on 3 pools of sorted GPI-deficient (GPI-) and GPI normal (GPI+) bone marrow cells derived from the same Pig-a knock-out animals, and identified 1275/669 genes of the 45,101 transcripts potentially available for screening using 2-fold change, <10% false discovery rate (FDR) and percentage of present calls as selection criteria. The major representative genes belong to the category of immune response. We tested whether the molecular differences between GPI- and GPI+ bone marrow cells could be preserved when GPI- cells were transplanted in lethally-irradiated wild type mice (C57BL/6). Microarray analysis was performed using sorted bone marrow cells from 4 animals transplanted with GPI-deficient bone marrow cells (T-GPI-) from Pig-a knock-out donors, 3 animals transplanted with GPI-normal bone marrow cells from C57BL/6 donors (T-GPI+), and GPI-normal bone marrow cells from 4 wild-type C57BL/6 mice (WT-GPI+). We found 296 probesets with 2-fold change cutoff, of which T-GPI- cells had 145 up-regulated genes in comparison to WT-GPI+ cells, and had 123 genes differentially expressed when compared to T-GPI+ cells. The gene expression of the GPI-deficient cells was very similar between the two sets of microarray experiments affirming the maintenance of the phenotype before and after bone marrow cell transplantation.

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C/EBPepsilon ChIP-sequencing of C57BL/6 mice bone marrow cells

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