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PRDM15 promotes lymphomagenesis by transcriptionally rewiring B cells metabolism

ABSTRACT: RNAseq of samples to identify changes in gene expression upon acute PRDM15 deletion

ORGANISM(S): Mus musculus

PROVIDER: GSE116906 | GEO | 2019/07/04

REPOSITORIES: GEO

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PRDM15 promotes lymphomagenesis by transcriptionally rewiring B cells metabolism

Project description:PRDM15 promotes lymphomagenesis by transcriptionally rewiring B cells metabolism

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RNAseq in immortalized human podocyte cell line following PRDM15 CRISPR knock-out

Project description:We recently identified variants in PRDM15 in affected individuals with proteinuric kidney disease. To determine the downstream pathways mediated by PRDM15 knock-down, PRDM15 knock-out immortalized podocyte cell lines were generated using CRISPR/Cas genome editing. Two different guide RNAs were utilized to generate two different cell lines, while a scramble guide RNA was utilized as control. We performed RNAseq and identified 151 differentially regulated genes, which coalesced upon pathways involved in renal development.

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PRDM15 is a key regulator of metabolism critical to sustain B-cell lymphomagenesis.

Project description: Not available

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PRDM15 mutation prevents forebrain development through an Otx2 pathway

Project description:Acquiring correct brain anatomy and function requires extensive morphogenesis and patterning, which is regulated by a complex gradient of transcription factors. Members of the PR domain containing (PRDM) chromatin-modulating family of transcriptional regulators function in neuronal specification and brain patterning. Little is known about the function of PRDM15, even though it is predicted to have a role in the development of the central nervous system, and lies in the Down syndrome trisomy region of HSA21 and MMU16. Here, we show that PRDM15 is required for forebrain development and repression of hindbrain gene expression. The phenotype of Prdm15 mutants mimics that of Otx2 loss. Using RNA sequencing, we found that a PRDM15 dependent molecular pathway, which includes many homeodomain factors that pattern the forebrain, including OTX2 and PAX6, is disrupted in Prdm15 mutants. Consistent with the role of OTX2 as a master regulator of forebrain development, which represses rostral expansion of the hindbrain to maintain the brain rostro-caudal axis, conditionally inactivating PRDM15 in the forebrain also truncates the forebrain and disrupts the brain rostro-caudal axis. PRDM15 co-expresses with OTX2 in cells of the primordial anterior forebrain, a region where OTX2 is known to function, and PRDM15 binds to the Otx2 promoter, suggesting it may directly impact Otx2 expression. These findings place PRDM15 in the forebrain transcriptional hierarchy for the first time, revealing that PRDM15 is a candidate for pathogenesis in Down syndrome or other neurodevelopmental disorders.

2020-08-06 | GSE97208 | GEO

Identification of PRDM15 cistrome in the mouse ESCs

Project description:Genome-wide binding sites of PRDM15 were identified in mouse ESCs

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Identification of PRDM15 Cistrome in Emu-Myc Lymphoma cells

Project description:Genome-wide binding targets of PRDM15 were identified in Emu-Myc Lymphomas

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Identification of PRDM15 cistrome in the mouse embryo (6.5 d.p.c)

Project description:Genome-wide binding sites of PRDM15 were identified in 6.5 d.p.c embryos

2019-12-25 | GSE125750 | GEO

Genome-wide mapping of PRDM15 binding in pluripotent mouse Embryonic Stem Cells (mESCs)

Project description:Genome-wide mapping of PRDM15 binding in pluripotent mouse Embryonic Stem Cells (mESCs)

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RNAseq in immortalized human podocyte cell line following PRDM15 CRISPR knock-out

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Partial loss of Rpl11 in adult mice recapitulates Diamond-Blackfan anemia (DBA) and promotes lymphomagenesis

Project description:Diamond-Blackfan anemia (DBA) is characterized by anemia and cancer susceptibility, and is caused by mutations in ribosomal genes, including Rpl11. Here, we report that Rpl11-heterozygous embryos are not viable, and homozygous deletion of Rpl11 in adult mice results in death within a few weeks, accompanied by bone marrow aplasia and intestinal atrophy. Importantly, deletion of a single Rpl11 allele in adult mice results in anemia associated to decreased erythroid progenitors and defective erythroid maturation. These phenotypes are also present in mice transplanted with inducible heterozygous Rpl11 bone marrow, indicating a cell-autonomous role of RPL11 in erythropoiesis. Additionally, fibroblasts lacking one or both Rpl11 alleles show defective p53 activation upon ribosomal stress or DNA damage. Furthermore, fibroblasts and hematopoietic tissues from heterozygous Rpl11 mice present higher basal cMYC levels. Accordingly, heterozygous Rpl11 mice are highly susceptible to radiation-induced lymphomagenesis. We conclude that Rpl11-deficient mice recapitulate DBA disorder, including cancer predisposition. RNAseq profiles of bone marrow hematopoietic progenitors cells from WT (Rpl11+/+:: Tg.UbC-CreERT2) and LOX (Rpl11+/lox::Tb.Ub-CreERT2) mice, n=4 independent animals per genotype

2015-09-01 | E-GEOD-72537 | biostudies-arrayexpress

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