Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1095989 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28545035_1.fastq.gz | Fastqsanger.gz | |||
| SRR28545035_2.fastq.gz | Fastqsanger.gz | |||
| SRR28545036_1.fastq.gz | Fastqsanger.gz | |||
| SRR28545036_2.fastq.gz | Fastqsanger.gz | |||
| SRR28545037_1.fastq.gz | Fastqsanger.gz |
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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:This SuperSeries is composed of the following subset Series: GSE41541: Expression data from mouse proximal intestinal epithelial Lgr5(hi) stem cells and differentiated villus cells (enterocytes from Atoh1 conditional knockout) GSE41542: H3K79me2 ChIP-seq in mouse proximal intestinal Lgr5(hi) stem cells and villus cells GSE41710: Global gene expression analysis of Dot1l-deficient and control intestinal villus cells in mouse Refer to individual Series
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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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