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Analysis of Blimp-1 and Irf-1 genomic binding in wild type and Prdm1/Blimp-1 mutant embryonic gut

ABSTRACT: The goal of this study was to profile Blimp1 binding in E18.5 small intestine using a Blimp-1-eGFP knock-in allele, and to compare Blimp-1-eGFP genomic binding with Irf-1 genomic binding in normal small intestine. Changes in Irf-1 binding between wild type and Prdm1/Blimp-1 mutant small intestine were also assessed. ChIP-seq was performed for Blimp-1-eGFP in duplicate in E18.5 small intestine expressing the fusion protein using anti-GFP antibody. As a negative control a single anti-GFP ChIP was also performed in wild type small intestine. ChIP-seq for Irf-1 was performed in duplicate in both wild type and Prdm1/Blimp-1 mutant E18.5 small intestine using an anti-Irf-1 antibody. Duplicate IgG ChIP control in wild types was performed as a negative control. All samples had an associated input chromatin sample sequenced.

ORGANISM(S): Mus musculus

SUBMITTER: Andrew Nelson

PROVIDER: E-GEOD-66069 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Blimp1/Prdm1 Functions in Opposition to Irf1 to Maintain Neonatal Tolerance during Postnatal Intestinal Maturation.

Mould Arne W AW Morgan Marc A J MA Nelson Andrew C AC Bikoff Elizabeth K EK Robertson Elizabeth J EJ

PLoS genetics 20150709 7

The neonatal intestine is a very complex and dynamic organ that must rapidly adapt and remodel in response to a barrage of environmental stimuli during the first few postnatal weeks. Recent studies demonstrate that the zinc finger transcriptional repressor Blimp1/Prdm1 plays an essential role governing postnatal reprogramming of intestinal enterocytes during this period. Functional loss results in global changes in gene expression patterns, particularly in genes associated with metabolic functio ...[more]

PMID: 26158850

Similar Datasets

Analysis of Blimp-1 and Irf-1 genomic binding in wild type and Prdm1/Blimp-1 mutant embryonic gut

Project description:The goal of this study was to profile Blimp1 binding in E18.5 small intestine using a Blimp-1-eGFP knock-in allele, and to compare Blimp-1-eGFP genomic binding with Irf-1 genomic binding in normal small intestine. Changes in Irf-1 binding between wild type and Prdm1/Blimp-1 mutant small intestine were also assessed.

2015-07-10 | GSE66069 | GEO

The transcriptional repressor Blimp1/Prdm1 regulates post-natal reprogramming of intestinal enterocytes

Project description:Expression profiling of Prdm1 mutant E18.5 small intestine was performed using Illumina whole genome V2 arrays. The hypothesis tested in the present study was that Blimp1 regulates the transcription of key genes involved in enterocyte differentiation and survival. Results identify substantial and premature activation of key components of the adult enterocyte biochemical signature. Villin-Cre and Prdm1BEH/+ animals were intercrossed to generate heterozygous Villin-Cre, Prdm1BEH males that were then mated with homozygous Prdm1 CA/CA females carrying the R26R allele to generate Prdm1+/+ (Prdm1CA/+) or Prdm1-/- (Villin-Cre, Prdm1CA/BEH) offspring. Total RNA obtained from 11 Prdm1+/+ and 10 Prdm1-/- E18.5 small intestine samples was hybridized to Illumina WG6_V2 beadchips.

2011-06-02 | E-GEOD-29658 | biostudies-arrayexpress

Comparison of the transcripts in control and Blimp-1-deficient keratinocytes

Project description:We performed microarray analysis to examine the differential gene expression profiles between Prdm1 (Blimp-1)-deleted and control keratinocytes. Keratinocytes isolated from Prdm1-floxed K5-CreER positive (CKO) mice were cultured in the presence of 4OHT to induce deletion of the Prdm1 allele in vitro. Prdm1-floxed K5-CreER positive (CKO) keratinocytes treated with the ethanol solvent control (EtOH) or Prdm1-floxed K5-CreER negative (control) keratinocytes treated with 4OHT or EtOH served as controls. Microarray analyses revealed that there were 93 genes up-regulated and 109 genes down-regulated by more than 2-fold in the CKO + 4OHT group in comparison with the CKO + EtOH, Ctrl + 4OHT or Ctrl + EtOH groups. Several corneocytes-related genes, including Rptn, Lce1f, Krt1 and Lce1d, are significantly down-regulated and several cytokines/chemokines, including Cxcl1, Cxcl2, Cxcl5 and Il24, are significantly up-regulated upon the deletion of Prdm1 in vitro. We analyzed the transcription profiles in control and Blimp-1-deficient keratinocytes using the GeneChipÂ® Mouse Expression Array 430A.

2013-04-02 | E-GEOD-34586 | biostudies-arrayexpress

Gene expression in LCMV-specific Blimp-1 deficient effector CD8+ T cells compared to wildtype effector CD8+ T cells

Project description:Antigen-specific effector CD8+ T cells deficient in Blimp-1 (Prdm1) do not acquire maximal effector functions, evade terminal differentiation, and more rapidly acquire some hallmark properties of memory CD8+ T cells. In this study, we compared the gene expression profiles of wildtype and Prdm1-/- LCMV-specific effector CD8+ T cells to better understand the molecular mechanisms underlying this striking phenotype. DNA microarray analysis was performed of DbGP33-41 and DbNP396-404 tetramer-positive effector CD8+ T cells FACS-sorted at day 8 post-LCMV infection from four independent samples of either Blimp-1 conditional knockout mice (CKO; Blimp-1flox/flox x GranzymeB-cre+) or wildtype (WT) littermate controls.

2010-08-19 | E-GEOD-17211 | biostudies-arrayexpress

VillinCre-Blimpflox mice postpartum day 7

Project description:In many mammalian species, the intestinal epithelium is immature at birth. During the suckling to weaning transition, the intestine matures. This developmental transition is the result of a genetic program that is intrinsic to the gut and independent of luminal content, but its regulators have not been identified. We investigated the function of the transcriptional repressor Blimp-1 using mice with intestine-specific ablation of Blimp-1. Deletion of Blimp-1 results in growth retardation and excess neonatal mortality. Mutant mice lack all typical epithelial features of the suckling period and are born with features of adult-like intestine. To assess the function of the gene Prdm1 (Blimp) on postnatal day 7 intestinal epithelium, VillinCre-Blimpflox and control (VillinCre-Blimpwt or Cre-Blimpflox) mice were generated. Mice were sacrificed at day 7 postnatal, and pieces of whole mid-intestine were taken for analysis.

2011-07-17 | E-GEOD-30556 | biostudies-arrayexpress

Comparison of the transcripts in control and Blimp-1-deficient keratinocytes

2013-04-02 | GSE34586 | GEO

Mus musculus

Project description:Analysis of Blimp-1 and Irf-1 genomic binding in wild type and Prdm1/Blimp-1 mutant embryonic gut

| PRJNA276077 | ENA

Gene expression in LCMV-specific Blimp-1 deficient effector CD8+ T cells compared to wildtype effector CD8+ T cells

2009-07-22 | GSE17211 | GEO

The transcriptional repressor Blimp1/Prdm1 regulates post-natal reprogramming of intestinal enterocytes

2011-06-02 | GSE29658 | GEO

BLIMP-1 is insufficient to induce antibody secretion in the absence of IRF4

Project description:Differentiation of B cells into antibody secreting cells (ASCs), plasmablasts and plasma cells, is regulated by a network of transcription factors. Within this network factors including PAX5 and BCL6 prevent ASC differentiation and maintain the B cell phenotype whereas BLIMP-1 and high IRF4 expression promote plasmacytic differentiation. BLIMP-1 is thought to induce immunoglobulin secretion. While IRF4 is needed for the survival of ASCs, its role in the regulation of antibody secretion has been controversial. BCL6-deficient DT40 B cell line has upregulated BLIMP-1 expression and secrete antibodies. In order to study the role of IRF4 in regulation of antibody secretion we have created a double knockout (DKO) DT40 B cell line deficient in both IRF4 and BCL6. This DKO cell line did not upregulate PRDM1 (the gene encoding for BLIMP-1) expression or secrete IgM. Even enforced BLIMP-1 expression in DKO cells or IRF4-deficient cells could not induce IgM secretion while it did in WT cells. However, enforced IRF4 expression in DKO cells induced strong IgM secretion. Our findings support a model where IRF4 expression in addition to BLIMP-1 expression is required to induce antibody secretion.

2018-03-05 | GSE94836 | GEO

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