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

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

PROVIDER: PRJNA432778 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6666085.fastq.gz	Fastqsanger.gz
	SRR6666086.fastq.gz	Fastqsanger.gz
	SRR6666087.fastq.gz	Fastqsanger.gz
	SRR6666088.fastq.gz	Fastqsanger.gz

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PRMT1 and CSNK1a1 control epidermal progenitor maintenance

Project description:PRMT1 and CSNK1a1 control epidermal progenitor maintenance

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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 (PRMT1/CSNK1a1 transcriptome profiling data sets)

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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.

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ID1 and CEBPA coordinate epidermal progenitor cell

Project description:The regulatory circuits that coordinate epidermal differentiation during development are still not fully understood. Here we report that the transcriptional regulator ID1 is enriched in basal epidermal progenitor cells and find ID1 expression to be diminished upon differentiation. In utero silencing of Id1 impairs progenitor cell proliferation, leads to precocious delamination of targeted progenitor cells and enables differentiated keratinocytes to retain progenitor markers and characteristics. Transcriptional profiling suggests ID1 acts by mediating adhesion to the basement membrane while inhibiting spinous layer differentiation. Co-immunoprecipitation reveals ID1 binding to transcriptional regulators of the class I bHLH family. We localize bHLH Tcf3, Tcf4 and Tcf12 to epidermal progenitor cells during epidermal stratification and established TCF3 as a downstream effector of ID1-mediated epidermal proliferation. Finally, we identify crosstalk between CEBPA, a known mediator of epidermal differentiation, and Id1 and demonstrate that CEBPA antagonizes BMP-induced activation of Id1. Our work establishes ID1 as a key coordinator of epidermal development, acting to balance progenitor proliferation with differentiation and unveils how functional crosstalk between CEBPA and Id1 orchestrates epidermal lineage progression.

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Identification of PRMT1 interaction proteins in cancer and neural stem cells

Project description:We have showed that cancer cells (or tumorigenic cells) resemble neural stem/progenitor cells in regulatory network, tumorigenicity and differentiation potential. We have shown PRMT1 is a protein that is upreguated in and promotes vaious cancers. The expression of its gene is localized to embryonic neural cells during vertebrate embryogenesis. The project is to identify the interaction partners of PRMT1, by which PRMT1 regulates neural stemness in both cancer cells and neural stem cells.

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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

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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Targeting epigenetic networks mediated by Prmt1 and Kdm4c in acute myeloid leukemia

Project description:Transcriptional deregulation plays a major role in acute myeloid leukemia, identification of epigenetic modifying enzymes essential for the maintenance of oncogenic transcription programs holds the key to better understanding the biology and designing effective therapeutic strategies for the disease. Here we provide experimental evidence showing the functional involvement and therapeutic potentials of targeting PRMT1 with H4R3 methyltransferase activity in various MLL and non-MLL leukemias. PRMT1 is necessary but not sufficient for leukemic transformation, which requires co-recruitment of KDM4C with H3K9 demethylase activity by chimeric transcription factors to mediate epigenetic reprogramming. Inhibition of KDM4C/PRMT1 suppresses transcription and transformation ability of MLL fusions and MOZ-TIF2, revealing a novel and targetable epigenetic circuitry mediated by PRMT1 and KDM4C in acute leukemia.

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