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Comprehensive transcriptome analysis of the brain in CNS-specific PRMT1 knockout mice.

ABSTRACT: Comprehensive transcriptome analysis of the brain in CNS-specific PRMT1 knockout mice.

PROVIDER: PRJNA521062 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8535060_1.fastq.gz	Fastqsanger.gz
	SRR8535060_2.fastq.gz	Fastqsanger.gz
	SRR8535070_1.fastq.gz	Fastqsanger.gz
	SRR8535070_2.fastq.gz	Fastqsanger.gz
	SRR8535061_1.fastq.gz	Fastqsanger.gz

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Comprehensive transcriptome analysis of the brain in CNS-specific PRMT1 knockout mice.

Project description:Arginine methylation is a common post-translation modification that is catalyzed by protein arginine methyltransferases (PRMTs). We generated the central nervous system-specific PRMT1 deficient (PRMT1-CKO) mice by Cre-loxP recombination system. Recently, we have discovered that PRMT1 is essential for development of CNS, and it is especially crucial for oligodendrocyte lineage progression and the subsequent myelination. In this study, we performed a comprehensive analysis of gene expression changes in whole brains, cortices or cerebella of wild type (WT) and PRMT1-CKO mice using RNA sequencing (RNA-seq). Filtering characteristics were used to identify the differentially expressed genes using the CLC Genomics Workbench software

2020-08-14 | GSE126127 | 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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Project description:Many studies investigated the mechanisms that control enteroendocrine cell (EEC) fate determination; however, regulation of EEC development and function are still unclear. Here, We performed RNA-Sequencing analyses on the small intestinal crypts of tamoxifen-inducible intestinal epithelium-specific knockout of PRMT1 and wildtype mice. Our finding for the first time revealed that the epigenetic enzyme PRMT1 controls mouse enteroendocrine cell differentiation, which probably via inhibition of Neurogenin 3-mediated commitment to the EEC lineage.

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Project description:We found that cardiomyocyte-specific PRMT1-deficient (PRMT1-cKO) mice showed dilated cardiomyopathy and aberrant cardiac alternative splicing. To identify novel cardiac splicing events, we performed a comprehensive analysis of gene expression changes in hearts of wildtype (WT) and PRMT1-cKO mice using RNA sequencing (RNA-Seq). To investigate differentially expressed genes (false discovery rate (FDR) p<0.05, fold change >2) between control and PRMT1-cKO mice, we performed pairwise comparisons of RNA-Seq data using the CLC Genomics Workbench software.

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The arginine methyltransferase PRMT1 establishes transcriptomic homeostasis essential for spermatogonial differentiation and male fertility

Project description:Protein arginine methyltransferase 1 (Prmt1) is known as the major Type-I protein arginine methyltransferase that deposits asymmetrical dimethylarginine (ADMA) in both histone and non-histone substrates. Nonetheless, how Prmt1 and its downstream signalling through substrate methylation function in the male germline development remains poorly understood. In this study, we discovered that Prmt1 is predominantly present in the spermatogonial population during mouse spermatogenesis. Using three Cre-mediated conditional Prmt1 knockout mouse lines, we observed that Prmt1 is essential for the maintenance of spermatogonial cells and Prmt1-deposited ADMA marks coordinate an inherent homeostasis among three types of substrate methylation. In conjunction with high-throughput Cut&Tag and modified mini-bulk Smart-seq2 analyses, we unveiled that Prmt1-mediated H4R3me2a mark enriched in the promoter region, together with other histone arginine methylations, drives a global transcriptomic landscape that maintains the regular gene expression and alternative splicing. Collectively, we provide the genetic evidence showing the essential role of Prmt1-deposited arginine methylation in the establishment of transcriptional homeostasis, and shed light on the methylarginine signalling pathway in orchestrating spermatogonial development in the mammalian germline.

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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

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