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Blimp1/Prdm1 is required for uterine remodeling and repair in the mouse following RU486-induced abortion

ABSTRACT: Blimp1/Prdm1 is required for uterine remodeling and repair in the mouse following RU486-induced abortion

PROVIDER: PRJNA1047184 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27007300_1.fastq.gz	Fastqsanger.gz
	SRR27007300_2.fastq.gz	Fastqsanger.gz
	SRR27007301_1.fastq.gz	Fastqsanger.gz
	SRR27007301_2.fastq.gz	Fastqsanger.gz
	SRR27007302_1.fastq.gz	Fastqsanger.gz

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Blimp1/Prdm1 is required for uterine remodeling and repair in the mouse following RU486-induced abortion

Project description:Transcriptional profiling of E6.0 wild type and Blimp1 mutant decidua, 14 hours after intraperitoneal injection with RU486 or mineral oil with was performed using RNA-seq to identify the role of Blimp1 in uterine remodelling and repair post abortion.

2025-01-06 | GSE249112 | GEO

Molecular function of Prdm1/Blimp1 in trophoblast giant cell differentiation.

Project description:Expression profiling of wild-type and Prdm1 null mouse trophoblast giant cell cultures using Illumina whole genome mouse V2 arrays. The hypothesis tested was that Prdm1/Blimp1 regulates expression of genes required for spiral artery trophoblast giant cell function. Prdm1 null and littermate control wild-type trophoblast stem cell clones were generated from blastocyst outgrowths. Total RNA was obtained from multiple replicates of four wild-type TS cell clones and four Prdm1 null TS cell clones differenitated for zero, two, four and six days by growth factor withdrawal and hybridized to Illumina WG6_V2 arrays

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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.

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Molecular function of Prdm1/Blimp1 in trophoblast giant cell differentiation.

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Blimp1/Prdm1 governs terminal differentiation of endovascular trophoblast giant cells and defines multipotent progenitors in the developing placenta

Project description:Expression profiling of Prdm1 mutant E9.5 placenta 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 trophoblast differentiation. We demonstrate that the invading SpA-TGCs display robust Blimp1 expression and Blimp1 functional loss selectively disrupts specification of this discrete TGC sub-type. Transcriptional profiling experiments identified additional SpA-TGC lineage restricted marker genes that potentially regulate placental morphogenesis. Prdm1BEH/+ (Vincent et al., 2005) animals were intercrossed to generate null placental tissue. Total RNA obtained from 10 Prdm1+/+ and 11 Prdm1-/- E9.5 placenta samples was hybridized to Illumina WG6_V2 beadchips.

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

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BLIMP1 negatively regulates IL-2 signaling in T cells

Project description:IL-2 signaling sustains immune homeostasis by fine-tuning the balance between effector and regulatory T cells. Our genome-wide CRISPR knockout screen using IL-2-dependent cells derived from a patient with Adult T-cell Leukemia (ATL) showed enriched sgRNAs targeting PRDM1 (encoding BLIMP1). BLIMP1 inhibits IL-2 production in T cells; however, its role in IL-2 signaling remains unknown. Here, we show that Prdm1 overexpression decreased IL-2 signaling in CD4+ T cells, while its deletion enhanced IL-2 signaling during influenza infection. Adoptive transfer of Prdm1 CKO Tregs into Rag2-/- mice elevated IL-2 signaling in T-cell induced colitis. Moreover, CRISPR/Cas9-mediated PRDM1 deletion augmented IL-2 signaling in human CD4+ T cells and natural Tregs with BLIMP1 binding to key genes affecting IL-2 signaling. Furthermore, ATL cells from acute patients exhibited increased IL-2 signaling but reduced BLIMP1 induction. Thus, BLIMP1 represses IL-2 signaling in T cells which is critical in orchestrating normal and pathophysiological immune responses.

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