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The transcriptional repressor Blimp-1/Prdm1 controls the maternal decidual response during pregnancy

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE141613 | GEO | 2020/05/01

REPOSITORIES: GEO

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The transcriptional repressor Blimp-1/Prdm1 controls the maternal decidual response during pregnancy [RNA-seq]

Project description:Transcriptional profiling of E5.5 and E6.5 wild type and Blimp1 mutant decidua was performed using RNA-seq to identify maternal Blimp1 functions during pregnancy .

2020-05-01 | GSE141612 | GEO

The transcriptional repressor Blimp-1/Prdm1 controls the maternal decidual response during pregnancy [ChIP-seq]

Project description:To identify candidate Blimp1 target genes in maternal decidua we performed GFP antibody ChIP-seq analysis of E6.5 decidua from homozygous female EGFP-BLIMP1 mice that express an endogenous N-terminal EGFP-tagged Blimp1 protein (Mitani et al., 2017).

2020-05-01 | GSE141611 | GEO

The transcriptional repressor Blimp-1/Prdm1 controls the maternal decidual response during pregnancy

Project description:The transcriptional repressor Blimp-1/Prdm1 controls the maternal decidual response during pregnancy

| PRJNA594041 | ENA

The transcriptional repressor Blimp1/PRDM1 regulates the maternal decidual response in mice.

Project description:The transcriptional repressor Blimp1 controls cell fate decisions in the developing embryo and adult tissues. Here we describe Blimp1 expression and functional requirements within maternal uterine tissues during pregnancy. Expression is robustly up-regulated at early post-implantation stages in the primary decidual zone (PDZ) surrounding the embryo. Conditional inactivation results in defective formation of the PDZ barrier and abnormal trophectoderm invasion. RNA-Seq analysis demonstrates down-regulated expression of genes involved in cell adhesion and markers of decidualisation. In contrast, genes controlling immune responses including IFNγ are up-regulated. ChIP-Seq experiments identify candidate targets unique to the decidua as well as those shared across diverse cell types including a highly conserved peak at the Csf-1 gene promoter. Interestingly Blimp1 inactivation results in up-regulated Csf1 expression and macrophage recruitment into maternal decidual tissues. These results identify Blimp1 as a critical regulator of tissue remodelling and maternal tolerance during early stages of pregnancy.

| S-EPMC7270082 | biostudies-literature

The transcriptional repressor Blimp-1/Prdm1 controls the maternal decidual response during pregnancy [ChIP-seq]

Project description:The transcriptional repressor Blimp-1/Prdm1 controls the maternal decidual response during pregnancy [ChIP-seq]

| PRJNA594045 | ENA

The transcriptional repressor Blimp-1/Prdm1 controls the maternal decidual response during pregnancy [RNA-seq]

Project description:The transcriptional repressor Blimp-1/Prdm1 controls the maternal decidual response during pregnancy [RNA-seq]

| PRJNA594046 | ENA

PRDM1/Blimp-1 controls effector cytokine production in human NK cells.

Project description:NK cells are major effectors of the innate immune response through cytolysis and bridge to the adaptive immune response through cytokine release. The mediators of activation are well studied; however, little is known about the mechanisms that restrain activation. In this report, we demonstrate that the transcriptional repressor PRDM1 (also known as Blimp-1 or PRDI-BF1) is a critical negative regulator of NK function. Three distinct PRDM1 isoforms are selectively induced in the CD56(dim) NK population in response to activation. PRDM1 coordinately suppresses the release of IFN-?, TNF-?, and TNF-? through direct binding to multiple conserved regulatory regions. Ablation of PRDM1 expression leads to enhanced production of IFN-? and TNF-? but does not alter cytotoxicity, whereas overexpression blocks cytokine production. PRDM1 response elements are defined at the IFNG and TNF loci. Collectively, these data demonstrate a key role for PRDM1 in the negative regulation of NK activation and position PRDM1 as a common regulator of the adaptive and innate immune response.

| S-EPMC3864810 | biostudies-literature

Decidual immune response following COVID-19 during pregnancy varies by timing of maternal SARS-CoV-2 infection.

Project description:While COVID-19 infection during pregnancy is common, fetal transmission is rare, suggesting that intrauterine mechanisms form an effective blockade against SARS-CoV-2. Key among these is the decidual immune environment of the placenta. We hypothesize that decidual leukocytes are altered by maternal SARS-CoV-2 infection in pregnancy and that this decidual immune response is shaped by the timing of infection during gestation. To address this hypothesis, we collected decidua basalis tissues at delivery from women with symptomatic COVID-19 during second (2nd Tri COVID, n = 8) or third trimester (3rd Tri COVID, n = 8) and SARS-CoV-2-negative controls (Control, n = 8). Decidual natural killer (NK) cells, macrophages and T cells were evaluated using quantitative microscopy, and pro- and anti-inflammatory cytokine mRNA expression was evaluated using quantitative reverse transcriptase PCR (qRT-PCR). When compared with the Control group, decidual tissues from 3rd Tri COVID exhibited significantly increased macrophages, NK cells and T cells, whereas 2nd Tri COVID only had significantly increased T cells. In evaluating decidual cytokine expression, we noted that IL-6, IL-8, IL-10 and TNF-α were significantly correlated with macrophage cell abundance. However, in 2nd Tri COVID tissues, there was significant downregulation of IL-6, IL-8, IL-10, and TNF-α. Taken together, these results suggest innate and adaptive immune responses are present at the maternal-fetal interface in maternal SARS-CoV-2 infections late in pregnancy, and that infections earlier in pregnancy show evidence of a resolving immune response. Further studies are warranted to characterize the full scope of intrauterine immune responses in pregnancies affected by maternal COVID-19.

| S-EPMC8867981 | biostudies-literature

The transcriptional repressor Blimp1/Prdm1 regulates postnatal reprogramming of intestinal enterocytes.

Project description:Female mammals produce milk to feed their newborn offspring before teeth develop and permit the consumption of solid food. Intestinal enterocytes dramatically alter their biochemical signature during the suckling-to-weaning transition. The transcriptional repressor Blimp1 is strongly expressed in immature enterocytes in utero, but these are gradually replaced by Blimp1(-) crypt-derived adult enterocytes. Here we used a conditional inactivation strategy to eliminate Blimp1 function in the developing intestinal epithelium. There was no noticeable effect on gross morphology or formation of mature cell types before birth. However, survival of mutant neonates was severely compromised. Transcriptional profiling experiments reveal global changes in gene expression patterns. Key components of the adult enterocyte biochemical signature were substantially and prematurely activated. In contrast, those required for processing maternal milk were markedly reduced. Thus, we conclude Blimp1 governs the developmental switch responsible for postnatal intestinal maturation.

| S-EPMC3127883 | biostudies-literature

Blimp-1/Prdm1 alternative promoter usage during mouse development and plasma cell differentiation.

Project description:The zinc-finger PR domain transcriptional repressor Blimp-1/Prdm1 plays essential roles in primordial germ cell specification, placental, heart, and forelimb development, plasma cell differentiation, and T-cell homeostasis. The present experiments demonstrate that the mouse Prdm1 gene has three alternative promoter regions. All three alternative first exons splice directly to exon 3, containing the translational start codon. To examine possible cell-type-specific functional activities in vivo, we generated targeted deletions that selectively eliminate two of these transcriptional start sites. Remarkably, mice lacking the previously described first exon develop normally and are fertile. However, this region contains NF-kappaB binding sites, and as shown here, NF-kappaB signaling is required for Prdm1 induction. Thus, mutant B cells fail to express Prdm1 in response to lipopolysaccharide stimulation and lack the ability to become antibody-secreting cells. An alternative distal promoter located approximately 70 kb upstream, giving rise to transcripts strongly expressed in the yolk sac, is dispensable. Thus, the deletion of exon 1B has no noticeable effect on expression levels in the embryo or adult tissues. Collectively, these experiments provide insight into the organization of the Prdm1 gene and demonstrate that NF-kappaB is a key mediator of Prdm1 expression.

| S-EPMC2772737 | biostudies-literature

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