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.
Project description:The mechanisms of transcriptional regulation underlying human primordial germ cell differentiation are largely unknown. Transcriptional repressor Prdm1/Blimp1 is known to play a critical role in controlling germ cell specification in mice. We show that ectopic expression of PRDM1 in hESCs promotes the generation of cells exhibiting transcriptomic features of early primordial germ cells.
Project description:Prdm1 encodes the transcriptional repressor PRDM1/BLIMP1 and Prdm1 mutant mice are one of the rare mutant strains that do not develop whisker hair follicles while still displaying a pelage. We demonstrate that Lef1, a key mediator of the Wnt/Beta Catenin pathway, acts upstream of Prdm1 and identify a primate specific deletion of a Lef1 enhancer, Leaf. This loss may have been significant in the evolutionary process, leading to the progressive defunctionalization and disappearance of vibrissae in primates.
Project description:Prdm1 encodes the transcriptional repressor PRDM1/BLIMP1 and Prdm1 mutant mice are one of the rare mutant strains that do not develop whisker hair follicles while still displaying a pelage. We demonstrate that Lef1, a key mediator of the Wnt/Beta Catenin pathway, acts upstream of Prdm1 and identify a primate specific deletion of a Lef1 enhancer, Leaf. This loss may have been significant in the evolutionary process, leading to the progressive defunctionalization and disappearance of vibrissae in primates.
Project description:Transcriptional repressor Prdm1/Blimp1 is known to play a key role in controlling B ells differentiation and regulating IL-10 production in regulatory T cells. B10 cells is the main IL-10 producing B cells in mouse spleen. We found that B10 cells and IL-10+ B cell levels are increased in Prdm1-deficient mice. Here, we compared the gene expression profiles of B10 cells from Prdm1-deficient mice (Cko) and its control littermate mice (Ctrl) in steady state and stimulated with anti-CD40 antibody for 48 h.
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.
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
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.
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.
Project description:Blimp1 (Prdm1), the key determinant of primordial germ cells (PGC), plays a combinatorial role with Prdm14 during PGC specification from postimplantation epiblast cells. They together initiate epigenetic reprogramming in early germ cells towards an underlying pluripotent state, which is equivalent to embryonic stem cells (ESC). Whereas Prdm14 alone can promote reprogramming and is important for the propagation of the pluripotent state, it is not known if Blimp1 is similarly involved. Using a genetic approach, we demonstrate that Blimp1 is dispensable for the derivation and maintenance of ESC and postimplantation epiblast stem cells (EpiSC). Notably, Blimp1 is also dispensable for reprogramming EpiSC to ESC. Thus, while Blimp1 is obligatory for PGC specification, it is not required for the reversion of EpiSC to ESC, and for their maintenance thereafter. This study suggests that reprogramming, including that of somatic cells to ESC, may not entail an obligatory route through Blimp1 positive PGC-like state.
