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PRMT1 and CSNK1a1 control epidermal progenitor maintenance (PRMT1/CSNK1a1 transcriptome profiling data sets)

ABSTRACT: Here we determine the target gene sets controlled by PRMT1 or CSNK1a1 in maintaining the undifferentiated state of primary human keratinocytes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE110049 | GEO | 2018/02/02

REPOSITORIES: GEO

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PRMT1 and CSNK1a1 control epidermal progenitor maintenance (PRMT1/CSNK1a1 transcriptome profiling data sets)

Project description:PRMT1 and CSNK1a1 control epidermal progenitor maintenance (PRMT1/CSNK1a1 transcriptome profiling data sets)

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PRMT1 and CSNK1a1 control epidermal progenitor maintenance

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PRMT1 and CSNK1a1 control epidermal progenitor maintanence (PRMT1 ChIP-seq data set)

Project description:Here we determine the genome-wide binding sites of PRMT1 in primary human keratinocytes. We also investigated the impact of casein kinase inhibitor D4476 on PRMT1 genomic binding.

2018-02-02 | GSE110050 | GEO

PRMT1 and CSNK1a1 control epidermal progenitor maintanence (PRMT1 ChIP-seq data set)

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PRMT1 and CSNK1a1 control epidermal progenitor maintenance

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-01-25 | GSE81942 | GEO

CSNK1a1 Regulates PRMT1 to Maintain the Progenitor State in Self-Renewing Somatic Tissue.

Project description:Somatic progenitors sustain tissue self-renewal while suppressing premature differentiation. Protein arginine methyltransferases (PRMTs) affect many processes; however, their role in progenitor function is incompletely understood. PRMT1 was found to be the most highly expressed PRMT in epidermal progenitors and the most downregulated PRMT during differentiation. In targeted mouse knockouts and in long-term regenerated human mosaic epidermis in vivo, epidermal PRMT1 loss abolished progenitor self-renewal and led to premature differentiation. Mass spectrometry of the PRMT1 protein interactome identified the CSNK1a1 kinase, which also proved essential for progenitor maintenance. CSNK1a1 directly bound and phosphorylated PRMT1 to control its genomic targeting to PRMT1-sustained proliferation genes as well as PRMT1-suppressed differentiation genes. Among the latter were GRHL3, whose derepression was required for the premature differentiation seen with PRMT1 and CSNK1a1 loss. Maintenance of the progenitors thus requires cooperation by PRMT1 and CSNK1a1 to sustain proliferation gene expression and suppress premature differentiation driven by GRHL3.

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Targeting Csnk1a1 induces selective p53-dependant killing of leukemia stem cells

Project description:We found found that casein kinase 1 alpha (Csnk1a1), a serine threonine kinase and negative regulator of beta catenin, is essential for leukemia cells in vivo. We examined the effect of Csnk1a1 knowckdown by gene expression profiling in primary leukemia cells.

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Toxoplasma gondii arginine methyltransferase 1 (PRMT1) regulates parasite counting during tachyzoite cell division

Project description:PRMT1 is thought to be responsible for the majority of PRMT activity in Toxoplasma gondii, but its exact function is unknown. We generated T. gondii mutants lacking PRMT1 (∆prmt1) by deletion of the PRMT1 gene. ∆prmt1 parasites exhibit morphological defects during cell division and grow slowly, and this phenotype reverses in the complemented strain ∆prmt::PRMT1mRFP. PRMT1 localizes primarily in the cytoplasm with enrichment at the centrosome, and the strain lacking PRMT1 is unable to segregate progeny accurately. Unlike wild-type and complemented parasites, ∆prmt1 parasites have abnormal daughter buds, perturbed centrosome stoichiometry, and loss of synchronous replication. Whole genome expression profiling demonstrated differences in expression of cell cycle regulated genes in ∆prmt1 relative to the complemented ∆prmt1::PRMT1mRFP and parental wild-type strains, but these changes did not correlate with a specific block in cell cycle. Although PRMT1’s primary biological function was previously proposed to be methylation of histones, our genetic studies suggest that the most critical function of PRMT1 is within the centrosome as a regulator of daughter cell counting to assure the proper replication of the parasite. RNA samples were isolated in triplicates from RH-hxgprt parent strain (W), PRMT1 knockout (K) strain and PRMT1 knockout strain complemented with RFP-tagged PRMT1 protein (C). Parasites were grown for 32h at 37C. Samples were hybridized to the Toxoplasma gondii Affymetrix microarray (ToxoGeneChip: http://ancillary.toxodb.org/docs/Array-Tutorial.html). Hybridization data was preprocessed with Robust Multi-array Average (RMA) and normalized using per chip and per gene median polishing and analyzed using the software package GeneSpring GX (Agilent Technologies).

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Dissecting the stem cell compartment in Csnk1a1 haploinsufficiency

Project description:We sorted hematopoietic progenitors from mouse bone marrow previously transplanted with either Csnk1a1 fl/+ or Mx1Cre+ bone marrow and performed scRNAseq. We identified cell populations in a continuum of differentiation from quiescent stem cell to cycling lineage-marker expressing progenitor. Our analysis revealed signaling changes in primitive stem cells with Csnk1a1 haploinsufficiency that result in downregulation of inflammatory NFkB signaling while upregulating Myc and E2f dependent pro-proliferative pathways

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PRMT1-mediated FLT3 arginine methylation is required for maintenance of FLT3-ITD+ Acute Myeloid Leukemia

Project description:The presence of FLT3-ITD mutations in patients with acute myeloid leukemia (AML) is associated with poor clinical outcome. FLT3 tyrosine kinase inhibitors (TKIs), although effective in kinase ablation, do not eliminate FLT3-ITD+ leukemia stem cells (LSCs) which are potential sources of disease relapse, prompting us to ask whether FLT3-ITD protein regulates the AML LSCs survival through a kinase-independent mechanism. Here, we show that expression of PRMT1, the primary type I arginine methyltransferase, significantly increases in LSC-enriched CD34+CD38- populations relative to normal counterparts. Genetic PRMT1 depletion blocked AML CD34+ cell survival, and had more potent effects in AML cells from patients harboring FLT3-ITD. Our genome wide analysis of gene expression and PRMT1 conditional KO mouse study confirmed that PRMT1 preferentially cooperates with FLT3-ITD contributing to AML cell maintenance. Mechanistically, PRMT1 catalyzed FLT3-ITD protein methylation at arginines 972/973, and PRMT1 promoted leukemia cell growth in a FLT3 methylation-dependent manner. Moreover, effects of FLT3-ITD methylation in AML cells were in part due to crosstalk with FLT3-ITD phosphorylation at tyrosine 969 (Y969). Importantly, FLT3 methylation persisted in FLT3-ITD+ AML cells following TKI (AC220) treatment, indicating that methylation occurs independently of kinase activity. Finally, in both patient-derived xenograft (PDX) and murine AML models, combined administration of AC220 with a type I PRMT inhibitor (MS023) enhanced elimination of FLT3-ITD+ AML relative to AC220 treatment alone. Our study demonstrates that PRMT1-mediated FLT3 methylation promotes LSC activity and suggests that combining PRMT1 inhibition with FLT3 TKI treatment could be a promising approach to selectively target FLT3-ITD+ LSCs.

2021-11-10 | GSE122435 | GEO

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